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)

Between January 1990 and July 1997, in 15 maintenance dialyzed patients and in 3 patients after renal transplantation manifesting hyperparathyroidisms surgical treatment was performed. The diagnosis was based both on the estimation of serum PTH level, total and ionised calcium, phosphates, alkaline phosphatase and imaging procedures: ultrasonography and 99-mTc subtraction scintigraphy. Indications to surgical treatment included ailments like generalized prurigo, bone and joint pains and muscular weakness with no response to pharmacological treatment. The commonly used procedure was subtotal parathyroidectomy (94%), its extent, however, was in each case determined during surgery, depending on the quantity and size of parathyroid glands found. In all cases the immediate intraoperative histopathological examination of the resected tissues was performed. In 10 patients resection of the thyroid gland tissues was carried out because of goiter (56%), among them in 1 case occult papillar carcinoma was found in histopathological examination. In the postoperative period 4 patients (22%) manifested transient hypocalcemia with good response to pharmacological treatment. Good results of surgical treatment reflected by both ailment relief and normalization of serum PTH and phosphates were obtained in 16 patients (89%). In 2 patients (11%) the ailments subsided but did not completely disappear. Surgical treatment of secondary hyperparathyroidism by subtotal parathyroidectomy is efficacious and entails a low risk of complications.
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PMID:[Surgical treatment of secondary hyperparathyroidism in patients treated with renal replacement]. 959 51

In patients suffering from hyperthyroidism dependent on Graves' disease, a reduction in Na+,K+ATPase activity has been demonstrated in red blood cells (RBCs), as well as an inverse correlation between this enzymatic action and free triiodothyronine (FT3) levels. The restoration of normal FT3 values also brings about a normalization of Na+,K+ATPase activity in erythrocytes. These results have made it possible to hypothesize that the thyroid hormones control Na+,K+ATPase activity and that this control is manifested by means of variations in the number of ouabain-binding sites. For this reason, the measurement of the activity of the Na/K pump can be considered as a further indicator of the peripheral effects of thyroid hormones. With a view to assess the relation between the course of treated hyperthyroidism and Na+,K+ATPase activity during antithyroid therapy and after surgical thyroidectomy followed by replacement therapy, we studied 24 patients affected by Graves' disease (group Graves [GG]). They were compared with 24 female Graves' patients who underwent total thyroidectomy for nontoxic and diffuse nodular goiter (NDNG) (group control [GC]) and with 24 normal healthy women (group normal [GN]). When Graves' hyperthyroidism was diagnosed, the Na+,K+ATPase activity in RBCs was impaired in all GG patients. Thionamide treatment restored the normal activity of the Na/K pump, accompanied by normalization of the number of ouabain-binding sites. One hundred eighty days after thyroidectomy, in conditions of clinical and biochemical euthyroidism due to replacement therapy with levothyroxine, the activity of Na+,K+ATPase in RBCs was once again reduced in GG, while appearing normal in GC and GN (1.77 +/- 0.16 mmol Pi h(-1) L(-1) RBCs v 2.09 +/- 0.26 v 2.09 +/- 0.24, P < .05). Different instrumental or biochemical parameters, such as glycemia, serum lipids, ions, serum alkaline phosphatase (AIPh), serum creatine phosphokinase (CPK), blood pressure, and heart rate, were evaluated and appeared normalized in GG and GC 180 days after surgery. We conclude that (1) in patients suffering from Graves' disease, subjected to total thyroidectomy followed by levothyroxine replacement therapy, there is a reduction in the activity of the Na+,K+ATPase on erythrocytes 6 months after the surgical approach; and (2) a similar alteration is not observed in patients subjected to thyroidectomy for NDNG. These findings allow the formulation of the hypothesis that (1) treatment with levothyroxine for 180 days after thyroidectomy in GG is not long enough to restore the normality of all the peripheral indicators of action of the thyroid hormones; and (2) levothyroxine replacement therapy is unable to guarantee euthyroidism in all the tissues in GG (eg, during hematopoiesis in the bone marrow).
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PMID:Impaired Na+,K+ATPase activity in red blood cells in euthyroid women treated with levothyroxine after total thyroidectomy for Graves' disease. 978 20

The authors reported a twelve year and four-month old girl who had prolonged fever for 2 weeks. Physical examination revealed a painless enlarged thyroid gland with firm consistency. Hyperparathyroidism was suspected because of hypercalcemia, hypophosphatemia, high level of serum alkaline phosphatase, and decreased density of long bones. Thyroid scan showed a cold nodule of the left upper lobe which subsequently proved to be a medullary thyroid carcinoma by high serum thyrocalcitonin level and pathological examination. Her 24-hour urinary vanillyl mandelic acid was in the normal range, and abdominal ultrasonography demonstrated normal adrenal glands. Multiple endocrine neoplasia type IIa (MEN IIa) was diagnosed by medullary thyroid carcinoma and hyperparathyroidism. However, the fully developed syndrome is characterized by the combined occurrence of medullary thyroid carcinoma, primary hyperparathyroidism, and pheochromocytomas. This syndrome is a rare, complex, and potentially lethal disease so early recognition and family screening are very important.
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PMID:Multiple endocrine neoplasia type IIa: a case report. 980 71

The molecules of the B7 family play a major role in T-lymphocyte costimulation through interaction with their counterreceptors CD28 and CTLA4. In the present study, we analyzed the possible expression of B7 molecules on surgically removed thyroid tissue of patients with autoimmune [Hashimoto's thyroiditis (HT) or Graves' disease (GD)] or nonautoimmune [nontoxic goiter (NTG) or papillary cancer (PC)] thyroid diseases. We found clear positivity of thyroid follicular cells for B7.1 in HT but not in GD, nor in nonautoimmune specimens (NTG, PC) using in situ analysis by alkaline phosphatase anti-alkaline phosphatase (APAAP) technique. Double immunostaining experiments in combination with an anti-human thyroglobulin antibody confirmed follicular B7.1 localization. On the contrary, no follicular B7.2 expression was observed in any specimen analyzed. These findings were confirmed by immunofluorescence flow cytometry on isolated follicular cells. The cytokines IL1beta and LPS were able to induce de novo B7.1 expression on cultured thyroid follicular cells. Intrathyroid T cells proved responsive to stimulation via the B7 ligand CD28, even in the absence of IL2. Moreover preliminary evidence was obtained for an inhibitory effect of anti-B7.1 mAb on T-cell proliferation in coculture with isolated thyroid follicular cells. It is conceivable that in HT, expression of B7.1 on follicular cells, together with MHC class II antigens and ICAM1, could provide a local costimulatory signal for T-lymphocyte differentiation toward the type 1 cytokine secretion pattern and maintenance of the autoimmune process.
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PMID:B7.1 costimulatory molecule is expressed on thyroid follicular cells in Hashimoto's thyroiditis, but not in Graves' disease. 981 3

Cultured thyroid epithelial cells can be induced to express intercellular adhesion molecule-1 (ICAM-1, or CD54). However, constitutive follicular expression of ICAM-1 has been reported only in thyroid autoimmunity. We evaluated the expression of ICAM-1 mRNA and protein on thyroid tissue from different autoimmune thyroid diseases, and its relationship with other immunologically relevant surface markers, namely costimulatory molecules of B7 family. Thyroid tissue sections were obtained by surgically removed thyroid glands from 6 patients with Hashimoto's thyroiditis (HT), 6 with Graves' disease (GD) and 3 with multinodular nontoxic goiter. We used in situ hybridization to localize ICAM-1 mRNA, and immunohistochemical analysis by alkaline phosphatase anti-alkaline phosphatase (APAAP) method. We showed a clear hybridization pattern, localized in follicular cells, in sections of glands with HT. The hybridization pattern was far less pronounced in GD: no staining was apparent on follicular cells. These results were strictly consistent with those obtained by means of immunohistochemistry. Moreover, double-staining experiments demonstrated colocalization of ICAM-1 and B7.1 molecules in HT, whereas no B7.1 expression was observed in Graves' or in non-autoimmune thyroid diseases. These data agree with the hypothesis of distinct immunoregulatory phenomena and effector mechanisms in the 2 main autoimmune thyroid diseases.
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PMID:Different intrathyroid expression of intercellular adhesion molecule-1 (ICAM-1) in Hashimoto's thyroiditis and Graves' disease: analysis at mRNA level and association with B7.1 costimulatory molecule. 1193 73

Bone metabolism markers (bone alkaline phosphatase, ionized calcium, inorganic phosphorus, serum osteocalcin) and urinary excretion of hydroxyproline, Ca2+ and P after overnight fasting and of creatinine were studied in 52 female patients with endemic goiter and hypothyrosis (18 of these with decompensated hypothyrosis, 34 treated with thyroid hormones) and 48 women without thyroid diseases aged 45-60 years with menopause of no longer than 10 years (6.4 +/- 0.43 years). Clinical and x-ray examinations were carried out in all women; hormonal status, basal serum levels of parathyroid hormone and calcitonin were evaluated. A trend to deceleration of bone remodeling was detected in the patients with untreated hypothyrosis in comparison with women without thyroid disease. Signs of increased bone resorption were detected in patients with endemic goiter and hypothyrosis receiving substitute hormone therapy; this gave grounds to refer patients of menopausal age with endemic goiter and hypothyrosis treated with oral thyroxin for a long time to a group at a high risk of osteoporosis and bone fractures and to start preventive osteotropic therapy from the first day of substitute thyroid hormone therapy.
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PMID:[Calcium-phosphorus metabolism and bone metabolism in postmenopausal patients with the thyroid gland pathology]. 1198 Jan 36

3,5,3'-triiodothyroacetic acid (TRIAC) has been used to suppress pituitary TSH secretion with reported attenuation of extrapituitary effects. We investigated whether equivalent doses of T (3) and TRIAC preventing the induction of goiter by methimazole (MMI) had a different or similar impact on peripheral tissues, such as liver and bone. In particular, we compared the effects of both compounds on the activity of the hepatic thyroid hormone-responsive enzymes, malic enzyme and L-glicerol-3-P dehydrogenase; bone mineral density and biochemical parameters of bone turnover, such as bone alkaline phosphatase (b-ALP) and the carboxy-terminal telopeptide region of type I collagen (beta-CTX); and the activity of thyroid ornithine decarboxylase (ODC). We also compared the effects of T (3) and TRIAC on the involution of MMI-induced goiter. Our results showed that TRIAC was more effective than T (3) to reduce MMI-induced goiter in a short-term goiter involution assay. TRIAC increased hepatic enzymes activity and beta-CTX levels, a parameter of bone resorption, more than T (3). However, bone mineral density was not altered by either treatment. Both compounds even reduced ODC activity at doses that were not effective at the pituitary level. These results demonstrate increased TRIAC hepatic and antigoitrogenic activity compared to T (3). TRIAC induces an imbalance in bone remodeling without affecting bone mineral density. Further studies are required to clarify this point.
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PMID:Comparison of the effects of 3,5,3'-triiodothyroacetic Acid and triiodothyronine on goiter prevention and involution and on hepatic and skeletal parameters in rats. 1515 8

This study was aimed at evaluating serum osteoprotegerin (OPG) concentrations in a cohort of patients with hyperthyroidism before and after methimazole (MMI) treatment. One hundred fourteen hyperthyroid patients [93 with Graves disease (GD) and 21 with toxic nodular goitre (TNG)] and 68 matched for sex and age healthy subjects were evaluated for serum free-thyroxine (FT4), free-triiodiothyronine (FT3), thyrotropin (TSH), TSH receptor antibodies (TRAb), bone alkaline phosphatase (BALP), C-telopeptides of type-1 collagen (CrossLaps), OPG levels, and bone mineral density (BMD). In hyperthyroid patients, the biochemical evaluations were performed before and after 6 and 12 months of MMI treatment, whereas BMD was measured at baseline and after 12 months of treatment. Hyperthyroidism was more severe in GD than TNG patients. Serum OPG levels were found to be significantly higher in hyperthyroid patients than in the healthy subjects (4.3 pmol/l, range: 1.6-12.0, vs. 2.2 pmol/l, range: 1.4-6.0; P < 0.001), the values being higher in GD patients than TNG. A significant correlation between serum OPG levels and age was found in the healthy subjects (r: 0.48; P < 0.001) but not in hyperthyroid patients (r: -0.03; P = 0.8). In the healthy subjects, serum OPG levels were also positively correlated with both serum FT4 (r: 0.23; P = 0.03) and FT3 (r: 0.24; P = 0.04) levels. In hyperthyroid patients, however, serum OPG was still correlated with FT3 levels (r: 0.38; P < 0.001), whereas the correlation with serum FT4 was lost (r: 0.19; P = 0.06). In hyperthyroid patients, but not in the healthy subjects, serum OPG levels were correlated positively with CrossLaps (r: 0.20; P = 0.03) and negatively with BALP (r: -0.24; P = 0.01) and BMD (r: -0.33; P = 0.01). After 6 months of MMI treatment, serum OPG concentrations decreased significantly in TNG patients (from 3.5 pmol/l, range: 1.6-8.0, to 2.3 pmol/l, range: 1.0-4.3; P < 0.001), whereas a not significant change in OPG levels occurred in GD patients (from 4.8 pmol/l, range: 1.8-12.0, to 4.2 pmol/l, range: 1.0-14.0; P = 0.7). At Month 12 of treatment, serum OPG concentrations were significantly lower than those measured at baseline in both TNG (2.5 pmol/l, range: 1.0-3.1, vs. 3.5 pmol/l, range: 1.6-8.0; P < 0.001) and GD (2.1 pmol/l, range: 1.0-8.6, vs. 4.8 pmol/l, range: 1.8-12.0; P < 0.001). At this time, no significant differences in serum OPG, CrossLaps, and BALP values were found between patients and control subjects. At the end of follow-up, BMD was higher than those measured at baseline but still significantly lower than those measured in the control subjects. This study shows that hyperthyroid patients have serum OPG concentrations significantly higher in comparison with euthyroid subjects, in relation to thyroid hormone excess and high bone turnover. Medical treatment of hyperthyroidism normalizes serum OPG levels in temporal relationship with the normalization of bone metabolism markers, even in presence of persistent abnormal bone structure as determined by ultrasonography.
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PMID:High serum osteoprotegerin levels in patients with hyperthyroidism: effect of medical treatment. 1533 17

In this study, we present a case of mild PBC that had anti-p97/VCP. A 53-year-old woman had been suspected of having chronic liver disease since 1983. In 1998, she visited the clinic, complaining of struma and pruritus. Laboratory findings on the first visit showed elevated levels of alkaline phosphatase (ALP) 454 IU/l(110-360), gammaGTP 250IU/l(-45) and IgM 671mg/dl(35-220). A screening of anti-mitochondrial antibody test was positive at a 1:80 dilution. A liver biopsy specimen revealed PBC at Scheuer stage 1. Following a treatment of ursodeoxycolic acid (UDCA) 300mg/day for 6 months, AMA and IgM were reduced to 1:20 and 220mg/dl, respectively. However, she was found to have low titer of anti-p97/VCP antibodies, determined by immunoprecipitation of radiolabeled recombinant protein produced by in vitro translation and transcription of the full length p97 cDNA. She has continued to be clinically stable following administration of UDCA 300mg. A PBC patient with anti-p97/VCP antibody showed a milder clinical course, suggesting some beneficial role of this antibody.
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PMID:[Case of primary biliary cirrhosis patient with anti-p97/VCP antibodies presenting a mild clinical course]. 1572 86

The goals of this study were to evaluate the acute and sublethal toxicity of copper (Cu(2+)) on the marine gastropod, Onchidium struma, and to examine the utility of enzymatic parameters as indicators of Cu(2+) exposure. In a semistatic renewal test, the 96-hour median lethal concentration of Cu(2+) for O. struma, 74.80 mg/L, was higher than that for other intertidal species. The activities of the antioxidative enzymes, Cu/Zn superoxide dismutase (Cu/Zn-SOD) and catalase (CAT), and those of the metabolic enzymes-acid phosphatase (ACP), alkaline phosphatase (AKP), glutamic-oxaloacetic transaminase (GOT), and glutamic-pyruvic transaminase (GPT) -in both hepatopancreas and muscle were determined after a 1-week exposure to Cu(2+) (range 1.35 to 4.20 mg/L). The activities of both Cu/Zn-SOD and CAT were higher in hepatopancreas than muscle. In addition, there was a negative correlation between Cu(2+) concentration and Cu/Zn-SOD activity in hepatopancreas, whereas a positive correlation was observed for CAT activity. Concentration-dependent changes in ACP and AKP activity showed a similar trend in hepatopancreas, increasing then decreasing and, finally, a slight increase. In contrast, ACP activity was positively correlated with Cu(2+) across the concentration range tested. In both hepatopancreas and muscle, both GOT and GPT were activated by lower concentrations of Cu(2+) and inhibited at higher concentrations.
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PMID:Toxic effects of copper on antioxidative and metabolic enzymes of the marine gastropod, Onchidium struma. 1921 21


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