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

Eleven premenopausal women with uterine myoma who received 300 micrograms of intranasal Gn-RH agonist (buserelin) three times daily for 6 months participated in this study. Serum estradiol, some parameters related to calcium metabolism and bone mineral density of the lumbar vertebrae assessed by quantitative computerized tomography were evaluated prior to, at the end of and 3 months after the treatment. Hypo-estrogenism was sustained during the treatment period. Calcitonin levels decreased rapidly after the first 2 weeks of the treatment and the fasting urinary hydroxyproline to creatinine excretion value increased in 1 month. Both serum alkaline phosphatase and osteocalcin increased slightly during the treatment. The serum m-parathyroid hormone levels showed no significant changes. There was no significant reduction in the mean lumbar vertebral bone mineral content (BMC) at the end of the treatment, but 4 out of 11 cases showed a decrease in BMC, which returned to the pretreatment level in 3 months after the cessation of treatment. From these findings, this therapy appears to have some effects on calcium metabolism during medication, but no adverse ones in the 3 months after treatment.
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PMID:Calcium metabolism in premenopausal women treated by a Gn-RH agonist for uterine myoma. 196 83

Estrogen deficiency results in bone mass reduction of largely varying extent in postmenopausal females, indicating that additional mechanisms influence the response of bone. They are by no ways identified in either the animal experiment or under clinical conditions. In search for factors, conditioning the response of bone to estrogen deficiency, we have conducted a study in females under treatment with the GnRH agonist decapeptyl (D-Trp6-LHRH). This drug blocks ovarian function and was administered for treatment of endometriosis or uterine leiomyoma. We determined spinal (dual photon absorptiometry) and forearm (single photon absorptiometry) bone mineral density before and 3 and 6 months after the onset of therapy and measured biochemical parameters of bone metabolism. Our results showed an increase in bone turnover after initiation of estrogen deficiency, as indicated by the elevation of alkaline phosphatase and osteocalcin. This resulted in a secondary decrease in serum intact PTH and 1,25-dihydroxy-vitamin D3. Furthermore, we found a positive correlation between pretreatment values of serum 1,25-dihydroxyvitamin D3 as well as its decrease and the reduction in bone mass during GnRH agonist treatment. This demonstrates that the patients' metabolic conditions predict their response to estrogen deficiency.
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PMID:Bone mass reduction after estrogen deprivation by long-acting gonadotropin-releasing hormone agonists and its relation to pretreatment serum concentrations of 1,25-dihydroxyvitamin D3. 213 29

Oestrogen deficiency at the menopause is associated with changes in calcium and bone metabolism. Hypo-oestrogenism induced by the use of GnRH-agonists is clinically useful in the treatment of oestrogen-dependent diseases. This study was done to investigate calcium homeostasis and bone metabolism of pre-menopausal women in a GnRH-agonist-induced pseudo-menopause. Eighteen patients with endometriosis or uterine leiomyoma received monthly i.m. injections of 3.2 mg of long-acting D-Trp-6-LHRH over a 6-month period. Plasma oestradiol-17 beta and progesterone levels under treatment were significantly decreased to the levels of the early follicular phase. Plasma total calcium, serum osteocalcin and plasma alkaline phosphatase concentrations increased, while plasma phosphate levels did not change. Levels of 1,25-dihydroxyvitamin D3 decreased significantly, but 25-hydroxyvitamin D3 values remained constant. Trabecular bone mineral density of lumbar spine decreased continuously during the 6-month period. Nine women completed 6-9 months follow-up. In these women bone loss was reversible. Cortical bone measurements at the proximal radius showed no change during oestrogen deficiency. In conclusion, our findings demonstrate that GnRH-agonist-induced bone loss is reversible. Furthermore, they suggest that the state of pseudo-menopause induced by GnRH-agonist may serve as a model for further pathophysiological studies on calcium homeostasis and bone metabolism in the post-menopause.
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PMID:Reversible bone loss in women treated with GnRH-agonists for endometriosis and uterine leiomyoma. 252 52

Alkaline phosphatase from human uterine myoma was purified to homogeneity by butanol extraction, acetone precipitation, column chromatography on DEAE-cellulose, QAE-Sephadex and Con-A-Sepharose, gel filtration on Sephadex G-200 and preparative electrophoresis. The relative molecular mass (145 000), subunit mass (35 000), neutral sugars (7 micrograms/mg) and sialic acid (1 microgram/mg) content were estimated. pH optimum of the enzyme activity was 10.0-10.4, and Km for p-nitrophenyl phosphate was 0.23 mM. The enzyme was inhibited by Zn2+, phosphate, fluoride, EDTA and by treatment with neuraminidase. Mg2+ activated alkaline phosphatase and showed protective effect towards inhibition by EDTA and Zn2+. The uterine muscle alkaline phosphatase was also purified. It showed lower specific activity than myoma phosphatase, higher molecular mass (160 000) and subunit mass (76 400), higher neutral sugar and sialic acid content.
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PMID:Alkaline phosphatase from human uterine myoma. I. Purification and some properties. 642 57

Thirty postmenopausal women, including 26 with history of hysterectomy and bilateral salpingooophorectomy due to uterine myoma and 4 with natural menopause without any diseases were randomly allocated into two groups. Fifteen subjects received medroxyprogesterone acetate (MPA) 10 mg twice daily for three months, the other 15 received both MPA 10 mg twice daily and cyclopentylethinyl estriol (CEE3) 5 mg once a month for three months. Fasting urinary calcium/creatinine (Ca/Cr) and hydroxyproline/creatinine (OHpr/Cr) ratio, serum calcitonon (CT) and alkaline phosphatase (AKP) concentrations were measured before and after treatment in all subjects. The results showed that in both groups, the fasting urinary Ca/Cr and OHpr/Cr ratio reduced significantly, while serum CT and AKP increased significantly after treatment. The changes of these parameters were not significantly different between these two groups. These data indicated that progestin alone appeared effective in preventing postmenopausal osteoporosis.
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PMID:[The effects of progestin on the bone metabolism in postmenopausal women]. 779 43

Quantitative techniques in immunohistochemistry are needed, but they are rarely applied because of doubtful reproducibility. We have developed a method for the detection of collagen types I and III in situ. The method applied was a two-step immuno-alkaline phosphatase technique with visualization of the end-product with Fast Red. The staining intensity was measured with a microdensitometer and the results expressed as ratios. The method yielded results that were unaffected by variations in tissue section thickness but which were proportionally related to time and antigen concentrations. Leiomyoma tissue, with a ratio of collagen types I and III of approximately 1.0, was used to establish the appropriate dilutions of the antibodies, thus assuring identical optical densities. By having the leiomyoma tissue sections incubated together with the heart tissue specimens, leiomyoma tissue was also helpful in correcting deviations from the 1.0 ratio. Accurate measurements of collagen type I/III ratios in normal human heart specimens were obtained with the present quantitative immunohistochemical technique.
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PMID:Quantification in immunohistochemistry: the measurement of the ratios of collagen types I and II. 804 7

The hypoestrogenic state induced by gonadotropin-releasing hormone agonists (GnRHa) has been shown to be effective in the treatment of uterine leiomyomas but to induce bone loss. Estriol has been described to be a weak and short-acting estrogen without an increased risk of endometrial proliferation and hyperplasia. The purpose of this study was to evaluate whether treatment of uterine leiomyomata with GnRHa plus oral estriol add-back therapy could prevent bone loss, without deteriorating the therapeutic effect of GnRHa. Twelve premenopausal women with symptomatic uterine leiomyomas were randomized to receive either leuprolide acetate depot alone at a dose of 3.75 mg s.c. every month for 6 months (non add-back group; n = 6), or GnRHa for 6 months plus oral estriol 4 mg/day for 4 months commencing with the third GnRHa injection (add-back group; n = 6). In the add-back group, leiomyoma volume, as measured by transvaginal ultrasound, decreased to 59.1% of baseline at 2 months of GnRHa therapy with no significant change in size during the remaining treatment period. In contrast, it decreased to 31.3% of pretreatment size at the end of treatment in the non add-back group. The levels of bone metabolic markers such as CrossLaps, deoxypyridinoline, osteocalcin and bone-specific alkaline phosphatase, increased significantly throughout the treatment in the non add-back group, whereas they were suppressed by the add-back therapy. The bone mineral density of lumbar spine (L2-L4) as measured by dual-energy X-ray absorptiometry decreased significantly by 7.5% at the end of treatment in the non add-back group, but did not change significantly in the add-back group. In conclusion, GnRHa plus estriol add-back therapy might be considered for long-term treatment of uterine leiomyomata.
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PMID:Estriol add-back therapy in the long-acting gonadotropin-releasing hormone agonist treatment of uterine leiomyomata. 1068 31

Placental alkaline phosphatase (PLAP) is normally produced by primordial germ cells and syncytiotrophoblasts, and the detection of its expression has been useful in the diagnosis of germ cell tumors. We have recently observed PLAP immunoreactivity in normal human adult and fetal muscle tissue. Based on this observation, we explored the possible role of PLAP in the diagnosis of soft tissue tumors. A total of 271 tumors were studied. These included tumors with myogenic, neural, fibrous, myofibroblastic, lipomatous, neuroepithelial, perivascular, and epithelial differentiation. A formalin-fixed, paraffin-embedded section from each tumor was stained with PLAP monoclonal antibody using standard immunohistochemical methods preceded by antigen retrieval. In addition, western blotting with PLAP monoclonal antibodies was performed on fresh samples from a uterine leiomyoma, grossly normal myometrium, and placenta. Also, formalin-fixed sections of fetal skeletal muscle were labeled with double immunohistochemistry techniques using antibodies to myogenin and PLAP. Cytoplasmic PLAP reactivity was detected in all leiomyomas and rhabdomyosarcomas (100%), 7 of 15 (46%) leiomyosarcomas, 15 of 19 (79%) desmoplastic small round cell tumors, 2 of 15 (13%) gastrointestinal stromal tumors, 1 of 8 (13%) Wilms' tumors, 1 of 9 synovial sarcomas (9%), and 2 of 7 (29%) myofibroblastic tumors. No PLAP reactivity was detected in hyperplastic scars, nodular fasciitis, or the other remaining soft tissue and epithelial tumors. Double immunohistochemistry studies showed coexpression of myogenin and PLAP in fetal skeletal muscle cells, and western blot analysis showed a 70-kDa band in samples derived from grossly normal placenta, benign myometrium, and a uterine leiomyoma. PLAP immunoreactivity is detected in soft tissue tumors with known myogenic differentiation. PLAP immunoreactivity seems to relate to the degree of myogenic differentiation in soft tissue tumors and is more frequently expressed in cells with skeletal muscle differentiation and least in those with myofibroblastic features. The biologic function of PLAP in muscle and tumors with myogenic differentiation is unknown and merits further investigation. In addition to its role as a germ cell marker, PLAP may also be used as a myogenic marker in the diagnosis of soft tissue tumors.
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PMID:Detection and diagnostic utilization of placental alkaline phosphatase in muscular tissue and tumors with myogenic differentiation. 1912 Oct 94