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PGE and 19-OH PGE were assayed by means of a gaschromatographic method and the most important seminal parameters (volume, concentration, motility and morphology of spermatozoa) were evaluated in basal conditions and at the end of indomethacin treatment, at a daily oral dose of 100 mg for thirty days. Adropin prostaglandin levels following indomethacin was observed in both groups of patients but only in the group with high concentrations of prostanoid derivates the prostaglandin inhibition was correlated with a significant improvement in sperm count and motility.",{"EN":238,"VI":239},"Role of seminal prostaglandins in male fertility. II. Effects of prostaglandin synthesis inhibition on spermatogenesis in man","Vai trò của prostaglandin trong tinh dịch đối với khả năng sinh sản của nam giới. II. Ảnh hưởng của sự ức chế tổng hợp prostaglandin lên quá trình sinh tinh ở người",{"VOID":241},"Isidori A., Conte D., Laguzzi G., Giovenco P., Dondero F. Role of seminal prostaglandins in male fertility. I Relationship of prostaglandin E and 19-OHI prostaglandin E with seminal parameters. J. Endocrinol. Invest. 3:1, 1980.\nPadron R.S., Nodarse M. Effect of indomethacin on semen of infertile men. Int. J. Androl. 2:110, 1979.\nCarpenter M.P., Robinson R.D., Thuy L.P. Prostaglandin metabolism by human testis. Lipids 13: 308, 1978.\nCooper E., Kelly R.W. The measurement of E and 19 hydroxy E prostaglandins in human seminal plasma. Prostaglandins 10: 507, 1975.\nConte D., Laguzzi G. Gaschromatography assay of human seminal prostaglandins. Lab. Patol. Clin. 7:111, 1977.\nBelsey M.A., Moghissi K.S., Eliasson R., Pausen C.A., Gallegos A.D., Prasad M.R.N. Laboratory manual for the examination of human semen and semen-cervical mucus concentration. Press Concern, Singapore W.H.O., 1980.\nSchlegel W., Rotermud S., Färber G., Nieschlag E. The influence of prostaglandins on sperm motility. Prostaglandins 21: 87, 1981.\nAbbatiello E.R., Kaminsky M., Weisbroth S. The effect of prostaglandins and prostaglandin inhibitors on spermatogenesis. Int. J. Fertil. 20:177, 1975.\nAbbatiello E.R., Kaminsky M., Weisbroth S. The effect of prostaglandin F1 and F2 on spermatogenesis. Int. J. Fertil. 21: 82, 1976.\nSaksena S.K., Hunt D.M., Lau I.F. Effects of prostaglandin F2 on sperm count, sperm motility and fertilizing capacity in the male rabbit. Int. J. Androl. 2: 639, 1978.\nSaksena S.K., Lau I.F. Temporary sterility induced by intrascrotal deposition of silastic-polyvinylpyrrolidone-prostaglandin F2 tubes in the rabbit: effect on fetal survival after regain of fertility. Fertil. Steril. 32: 340, 1979.\nTierney W.J., Daly I.W., Abbatiello E.R. The effects of prostaglandins PGE2 and PGF2 on spermatogenesis in adult male Sprague-Dawley rats. Int. J. Fertil. 24: 206, 1979.\nDidolkar A.K., Roychowdhury D. Effect of prostaglandin A-1, E-2, and F-2 on spermatogenesis in rats. J. Reprod. Fertil. 58: 275, 1980.\nDidolkar A.K., Roychowdhury D. Effects of prostaglandins E-1, E-2, F-1 and F-2 on human sperm motility. Andrologia 12:135, 1980.\nBiswas N.M., Sanyal S., Patro P.B. Antispermatogenic effect of Aspirin and its prevention by Prostaglandin E2. Andrologia 10: 137, 1978.\nSanyal S., Patra P.B., Nag S., Biswas N.M. Augmentation of luteinizing hormone action by Prostaglandin E2 in the prevention of Antispermatogenetic effect of Indomethacin. Andrologia 12:179, 1980.\nDidolkar A.K., Patel P.B., Roychowdhury D. Effect of Aspirin on spermatogenesis in mature and immature rats. Int. J. Androl. 3:585, 1980.",{"VOID":243},"10.1007\u002FBF03348497","PUBLICATION",[246],"VI","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF03348497",[249,265,279,293,301,317,331],{"id":250,"sortIndex":19,"researcher":18,"roles":251,"affiliations":253,"properties":262,"displayName":264,"givenName":18,"familyName":18},"aa84883c-c998-469b-94f6-5bd05096d030",[252],"AUTHOR",[254],{"id":255,"sortIndex":19,"affiliation":256,"properties":18},"af7d1cd3-8f62-4cfb-8f27-973d06bf74cf",{"id":255,"createTime":18,"updateTime":18,"relativeEntities":257,"slug":18,"properties":258,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":261,"statistic":18},[],{"title":259},{"VI":260},"Cattedra di Andrologia, Istituto di Clinica Medica V, University of Roma “La Sapienza”, Roma, Italy",[],{"title":263},{"VI":264},"D. 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Previous data obtained with single blood sampling were controversial as to increased ACTH levels compensatory to the Cortisol fall. We have evaluated by chronobiological procedures the circadian profiles of plasma ACTH and Cortisol in three patients with Cushing’s disease before and after a six-month course of therapy with ketoconazole (600 mg daily). None of the patients complained of any adverse subjective reaction; in particular no sign or symptom of hypoadrenalism and\u002For hepatotoxicity was recorded. Ketoconazole treatment markedly improved the clinical setting and caused a highly significant (p\u003C 0.0001) reduction of mean 24-h Cortisol values (ciradian MESOR). The expected rise of ACTH did not take place; rather, we detected a slight decrease of the mean circadian MESOR (p \u003C 0.05). Our data, althought obtained in a very small number of patients, suggest that ketoconazole may have an additional action at central level, at least in some cases of Cushing’s disease.",{"EN":411,"VI":412},"Ketoconazole treatment in Cushing’s disease. Effect on the circadian profile of plasma ACTH and Cortisol","Điều trị bệnh Cushing bằng ketoconazole. Ảnh hưởng lên biến thiên nhịp ngày đêm của ACTH và cortisol huyết tương",{"VOID":414},"Pont A., Williams P.L., Loose D.S., Feldman D., Rutz R.E., Bochra C., Stevens D.A. Ketoconazole blocks adrenal steroid synthesis. Ann. Intern. Med. 97: 370, 1982.\nLoose D.S., Kan P.B., Hirst M.A., Marcus R.A., Feldam D. Ketoconazole blocks adrenal steroidogenesis by inhibiting cytochrome P450-dependent enzymes. J. Clin. Invest. 77: 1495, 1983.\nKan P.B., Hirst M.A., Feldman D. Inhibition of steroidogenic cytochrome P450 enzymes in rat testis by ketoconazole and related imidazole antifungal drugs. J. Steroid Biochem. 23: 1023, 1985.\nNagai K., Miyamory I., Ideda M., Koshida H., Takeda R., Suhara K., Katagiri M. Effect of ketoconazole (an imidazole antimycotic agent) and other inhibitors of steroidogenesis on cytochrome P450-catalyzed reactions. J. Steroid Biochem. 24: 321, 1986.\nDe Felice R., Johsons D.J., Galgiani J.N. Gynecomastia with ketoconazole. Antimicrob. Agents Chemother. 19: 1073, 1981.\nTucker W.S., Snell B.B., Island D.P., Clarke R., Gregg M.D. Reversible adrenal insufficiency induced by ketoconazole. JAMA 253: 2413, 1985.\nMcCance D.R., Hadden D.R., Kennedy L., Sheridan B., Atkinson A.B. Clinical experience with ketoconazole as a therapy for patients with Cushing’s syndrome. Cliin. Endocrinol. (Oxf.) 27: 593, 1987.\nPont A., Garybill J.R., Craven P.C., Galgiani J.N., Dismukes W.E., Reitz R.E., Stevens D.A. High-dose ketoconazole therapy and adrenal and testicular function in humans. Arch. Intern. Med. 144: 2150, 1984.\nEngelhardt D., Mann K., Hormann R., Braun S., Karl H.J. Ketoconazole inhibits Cortisol secretion of an adrenal adenoma in vivo and in vitro. Klin. Wochenschr. 61: 373, 1983.\nAngeli A., Frairia R. Ketoconazole therapy in Cushing’s disease. Lancet 1: 821, 1985.\nContreras R., Rojas A., Blagini L., Gonzales P., Massardo T. Regression of metastatic adrenal carcinoma during palliative ketoconazole treatment. Lancet 2: 151, 1985.\nShepherd F.A., Hoffert B., Evans W.K., Emery G., Trachtenberg J. Ketoconazole use in the treatment of ectopic adrenocorticotropic hormone production and Cushing’s syndrome in small-cell lung cancer. Arch Intern. Med. 145: 863, 1985.\nSonino N., Boscaro M., Merola G., Mantero F. Prolonged treatment of Cushing’s disease by ketoconazole. J. Clin. Endocrinol. Metab. 61: 718, 1985.\nLoli P., Berselli M.E., Tagliaferri M. Use of ketoconazole in the treatment of Cushing’s syndrome. J. Clin. Endocrinol. Metab. 63: 1365, 1986.\nHalberg F., Tong Y.L., Johnson E.A. Circadian system phase. An aspect of temporal morphology; procedures and illustrative examples. In: Von Mayersbach H. (Ed.), The Cellular Aspects of Biorhythms. Springer Verlag, Berlin, 1967, p. 20\nAngeli A., Agrimonti F., Bertello P.D., Frairia R., Violino P.L., Barbadoro E., Ceresa F. Circadian patterns of plasma Cortisol and testosterone in chronic male alcoholics. Chronobiologia 9: 115, 1982.\nLewis J.H., Zimmerman H.J., Renson G.D., Ishak K.G. Hepatic injury associated with ketoconazole therapy. Gastroenterology 86: 503, 1984.\nBoscaro M., Sonino N., Rampazzo A., Mantero F. Response of pituitary-adrenal axis to corticotrophin releasing hormone in patients with Cushing’s disease before and after ketoconazole treatment. Clin. Endocrinol. (Oxf.) 27: 461, 1987.\nLoose D.S., Stover P., Feldman D. Ketoconazole binds to glucocorticoid receptors and exhibits glucocorticoid antagonist activity in cultured cells. J. Clin. Invest. 72: 404, 1983.\nStalla G.K., Stalla J., Huber M., Muller O.A. Ketoconazole inhibits cAMP generation and ACTH secretion in rat anterior pituitary cell culture. Acta Endocrinol. (Kbh.) 114: 32, 1987.\nBurrin J.M., Yeo T.H., Ashby M.J., Bloom S.R. Effect of ketoconazole on adrenocorticotrophic hormone secretion in vitro and in vivo. J. Endocrinol. 108: 37, 1986.\nNakamura M., Hirano M., Ibayashi H., Fujita T., Ohsawa N., Uchikawa T., Okinawa S., Kumamoto Y., Hirose K., Ichikawa T. A case of Cushing’s syndrome studied by urinary corticotrophin assay. Acta Endocrinol. (Kbh.) 42: 163, 1963.\nRefetoff S., Van Cauter E., Fang V.S., Laderman C., Graybeal M.L., Landau R.L. The effect of dexamethasone on the 24-hour profiles of adrenocorticotrophin and Cortisol in Cushing’s syndrome. J. Clin. Endocrinol. Metab. 60: 527, 1985.",{"VOID":416},"10.1007\u002FBF03350926","VERIFIED","2025-01-17T08:40:57.009+00:00","Auto Verify",[246],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF03350926",[423,438,451,464,477,490],{"id":424,"sortIndex":19,"researcher":18,"roles":425,"affiliations":426,"properties":435,"displayName":437,"givenName":18,"familyName":18},"61a55a96-abff-4837-9753-242381076b4a",[252],[427],{"id":428,"sortIndex":19,"affiliation":429,"properties":18},"346f9283-6d16-41e5-9c56-b691cb9609bb",{"id":428,"createTime":18,"updateTime":18,"relativeEntities":430,"slug":18,"properties":431,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":434,"statistic":18},[],{"title":432},{"VI":433},"Dipartimento di Biomedicina, Cattedra di Patologia Medica, Ospedale S. Luigi, Orbassano, Italy",[],{"title":436},{"VI":437},"M. Terzolo",{"id":439,"sortIndex":267,"researcher":18,"roles":440,"affiliations":441,"properties":448,"displayName":450,"givenName":18,"familyName":18},"f7e28913-677f-47f7-b115-44452d8c1f04",[252],[442],{"id":428,"sortIndex":19,"affiliation":443,"properties":18},{"id":428,"createTime":18,"updateTime":18,"relativeEntities":444,"slug":18,"properties":445,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":447,"statistic":18},[],{"title":446},{"VI":433},[],{"title":449},{"VI":450},"M. 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is widely accepted that type 2 amiodarone-induced thyrotoxicosis (AIT) generally occurs in patients with a normal thyroid gland without signs of thyroid autoimmunity. However, it is currently unknown if the presence of anti-thyroglobulin (TgAb) and\u002For anti-thyroperoxidase antibodies (TPOAb) in AIT patients without other signs of an underlying thyroid disease may impair the response to glucocorticoid therapy. We performed a pilot retrospective cohort study with matched-subject design and an equivalence hypothesis, comparing the response to glucocorticoid therapy between 20 AIT patients with a normal thyroid gland, low radioiodine uptake, undetectable TSH receptor antibodies and positive TgAb and\u002For TPOAb (Ab+ group), and 40 patients with the same features and absent thyroid antibodies (Ab− group). The mean cure time was 54 ± 68 days in the Ab+ group and 55 ± 49 days in the Ab− group (p = 0.63). The equivalence test revealed an equivalent cure rate after 60, 90 and 180 days (p = 0.67, 0.88 and 0.278, respectively). The occurrence of permanent hypothyroidism was higher in the Ab+ group than in the Ab− group (26.3 vs 5.13 %, p = 0.032). The presence of TgAb and\u002For TPOAb does not affect the response to glucocorticoid therapy, suggesting that the patients with features of destructive form of AIT should be considered as having a type 2 AIT irrespective of the presence of TGAb or TPOAb. These patients have a higher risk of developing hypothyroidism after the resolution of thyrotoxicosis and should be monitored accordingly.",{"EN":566,"VI":567},"The presence of anti-thyroglobulin (TgAb) and\u002For anti-thyroperoxidase antibodies (TPOAb) does not exclude the diagnosis of type 2 amiodarone-induced thyrotoxicosis","Sự hiện diện của kháng thể kháng thyroglobulin (TgAb) và\u002Fhoặc kháng thyroperoxidase (TPOAb) không loại trừ chẩn đoán nhiễm độc giáp do amiodarone type 2",{"EN":569},"",{"VOID":571},"Martino E, Bartalena L, Bogazzi F, Braverman LE (2001) The effects of amiodarone on the thyroid. Endocr Rev 22(2):240–254\nBogazzi F, Bartalena L, Gasperi M, Braverman LE, Martino E (2001) The various effects of amiodarone on thyroid function. Thyroid 11(5):511–519. doi:10.1089\u002F105072501300176471\nEskes SA, Wiersinga WM (2009) Amiodarone and thyroid. Best Pract Res Clin Endocrinol Metab 23(6):735–751. doi:10.1016\u002Fj.beem.2009.07.001\nBogazzi F, Tomisti L, Bartalena L, Aghini-Lombardi F, Martino E (2012) Amiodarone and the thyroid: a 2012 update. J Endocrinol Invest 35(3):340–348. doi:10.3275\u002F8298\nBarbesino G (2010) Drugs affecting thyroid function. Thyroid 20(7):763–770. doi:10.1089\u002Fthy.2010.1635\nBogazzi F, Bartalena L, Martino E (2010) Approach to the patient with amiodarone-induced thyrotoxicosis. J Clin Endocrinol Metab 95(6):2529–2535. doi:10.1210\u002Fjc.2010-0180\nBartalena L, Wiersinga WM, Tanda ML, Bogazzi F, Piantanida E, Lai A, Martino E (2004) Diagnosis and management of amiodarone-induced thyrotoxicosis in Europe: results of an international survey among members of the European Thyroid Association. Clin Endocrinol (Oxf) 61(4):494–502. doi:10.1111\u002Fj.1365-2265.2004.02119.x\nDiehl LA, Romaldini JH, Graf H, Bartalena L, Martino E, Albino CC, Wiersinga WM (2006) Management of amiodarone-induced thyrotoxicosis in Latin America: an electronic survey. Clin Endocrinol (Oxf) 65(4):433–438. doi:10.1111\u002Fj.1365-2265.2006.02590.x\nTanda ML, Piantanida E, Lai A, Liparulo L, Sassi L, Bogazzi F, Wiersinga WM, Braverman LE, Martino E, Bartalena L (2008) Diagnosis and management of amiodarone-induced thyrotoxicosis: similarities and differences between North American and European thyroidologists. Clin Endocrinol (Oxf) 69(5):812–818. doi:10.1111\u002Fj.1365-2265.2008.03268.x\nBogazzi F, Bartalena L, Tomisti L, Rossi G, Tanda ML, Dell’Unto E, Aghini-Lombardi F, Martino E (2007) Glucocorticoid response in amiodarone-induced thyrotoxicosis resulting from destructive thyroiditis is predicted by thyroid volume and serum free thyroid hormone concentrations. J Clin Endocrinol Metab 92(2):556–562. doi:10.1210\u002Fjc.2006-2059\nEaton SE, Euinton HA, Newman CM, Weetman AP, Bennet WM (2002) Clinical experience of amiodarone-induced thyrotoxicosis over a 3-year period: role of colour-flow Doppler sonography. Clin Endocrinol (Oxf) 56(1):33–38\nBogazzi F, Bartalena L, Tomisti L, Rossi G, Brogioni S, Martino E (2011) Continuation of amiodarone delays restoration of euthyroidism in patients with type 2 amiodarone-induced thyrotoxicosis treated with prednisone: a pilot study. J Clin Endocrinol Metab 96(11):3374–3380. doi:10.1210\u002Fjc.2011-1678\nBogazzi F, Bartalena L, Cosci C, Brogioni S, Dell’Unto E, Grasso L, Aghini-Lombardi F, Rossi G, Pinchera A, Braverman LE, Martino E (2003) Treatment of type II amiodarone-induced thyrotoxicosis by either iopanoic acid or glucocorticoids: a prospective, randomized study. J Clin Endocrinol Metab 88(5):1999–2002. doi:10.1210\u002Fjc.2002-021874\nChopra IJ, Baber K (2001) Use of oral cholecystographic agents in the treatment of amiodarone-induced hyperthyroidism. J Clin Endocrinol Metab 86(10):4707–4710. doi:10.1210\u002Fjcem.86.10.7976\nBrunn J, Block U, Ruf G, Bos I, Kunze WP, Scriba PC (1981) Volumetric analysis of thyroid lobes by real-time ultrasound (author’s transl). Dtsch Med Wochenschr 106(41):1338–1340. doi:10.1055\u002Fs-2008-1070506\nKnudsen N, Bols B, Bulow I, Jorgensen T, Perrild H, Ovesen L, Laurberg P (1999) Validation of ultrasonography of the thyroid gland for epidemiological purposes. Thyroid 9(11):1069–1074\nMosteller RD (1987) Simplified calculation of body-surface area. N Engl J Med 317(17):1098. doi:10.1056\u002FNEJM198710223171717\nGomez JM, Maravall FJ, Gomez N, Guma A, Soler J (2000) Determinants of thyroid volume as measured by ultrasonography in healthy adults randomly selected. Clin Endocrinol (Oxf) 53(5):629–634\nFranklyn JA, Gammage MD (2007) Treatment of amiodarone-associated thyrotoxicosis. Nat Clin Pract Endocrinol Metab 3(9):662–666. doi:10.1038\u002Fncpendmet0592\nTomisti L, Rossi G, Bartalena L, Martino E, Bogazzi F (2014) The onset time of amiodarone-induced thyrotoxicosis (AIT) depends on AIT type. Eur J Endocrinol 171(3):363–368. doi:10.1530\u002FEJE-14-0267\nBogazzi F, Bartalena L, Dell’Unto E, Tomisti L, Rossi G, Pepe P, Tanda ML, Grasso L, Macchia E, Aghini-Lombardi F, Pinchera A, Martino E (2007) Proportion of type 1 and type 2 amiodarone-induced thyrotoxicosis has changed over a 27-year period in Italy. Clin Endocrinol (Oxf) 67(4):533–537. doi:10.1111\u002Fj.1365-2265.2007.02920.x\nLatrofa F, Fiore E, Rago T, Antonangeli L, Montanelli L, Ricci D, Provenzale MA, Scutari M, Frigeri M, Tonacchera M, Vitti P (2013) Iodine contributes to thyroid autoimmunity in humans by unmasking a cryptic epitope on thyroglobulin. J Clin Endocrinol Metab 98(11):E1768–E1774. doi:10.1210\u002Fjc.2013-2912\nPedersen IB, Knudsen N, Carle A, Vejbjerg P, Jorgensen T, Perrild H, Ovesen L, Rasmussen LB, Laurberg P (2011) A cautious iodization programme bringing iodine intake to a low recommended level is associated with an increase in the prevalence of thyroid autoantibodies in the population. Clin Endocrinol (Oxf) 75(1):120–126. doi:10.1111\u002Fj.1365-2265.2011.04008.x\nSafran M, Martino E, Aghini-Lombardi F, Bartalena L, Balzano S, Pinchera A, Braverman LE (1988) Effect of amiodarone on circulating antithyroid antibodies. BMJ 297(6646):456–457\nForesti V, Pepe R, Parisio E, Scolari N, Zubani R, Bianco M (1989) Antithyroid antibodies during amiodarone treatment. Acta Endocrinol (Copenh) 121(2):203–206\nRotondi M, Coperchini F, Magri F, Chiovato L (2014) Serum-negative autoimmune thyroiditis: what’s in a name? J Endocrinol Invest 37(6):589–591. doi:10.1007\u002Fs40618-014-0083-8",{"VOID":573},"10.1007\u002Fs40618-015-0426-0","2024-12-24T01:46:01.458+00:00",[246],"https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002Fs40618-015-0426-0",[578,593,606,621,634,647,660,673,687,703,717,731],{"id":579,"sortIndex":19,"researcher":18,"roles":580,"affiliations":581,"properties":590,"displayName":592,"givenName":18,"familyName":18},"dd049223-6a29-4afd-b567-6b3e6acc6c8c",[252],[582],{"id":583,"sortIndex":19,"affiliation":584,"properties":18},"8e9969b3-0787-4991-9a33-a2516fe4aa3e",{"id":583,"createTime":18,"updateTime":18,"relativeEntities":585,"slug":18,"properties":586,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":589,"statistic":18},[],{"title":587},{"VI":588},"Endocrinology Unit, Department of Clinical and Experimental Medicine, University of Pisa, Pisa, Italy",[],{"title":591},{"VI":592},"L. 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Age Dordr 34:795–804. doi:10.1007\u002Fs11357-011-9280-y\nHarada K, Arita K, Kurisu K, Tahara H (2000) Telomerase activity and the expression of telomerase components in pituitary adenoma with malignant transformation. Surg Neurol 53:267–274\nHiraga S, Ohnishi T, Izumoto S, Miyahara E, Kanemura Y, Matsumura H, Arita N (1998) Telomerase activity and alterations in telomere length in human brain tumors. Cancer Res 58(10):2117–2125\nYoshino A, Katayama Y, Fukushima T, Watanabe T, Komine C, Yokoyama T, Kusama K, Moro I (2003) Telomerase activity in pituitary adenomas: significance of telomerase expression in predicting pituitary adenoma recurrence. J Neurooncol 63:155–162\nCury ML, Fernandes JC, Machado HR, Elias LL, Moreira AC, Castro M (2009) Non-functioning pituitary adenomas: clinical feature, laboratorial and imaging assessment, therapeutic management and outcome. Arq Bras Endocrinol Metab 53:31–39 (pii:S0004-27302009000100006)\nElias PC, Lugao HB, Pereira MC, Machado HR, Castro M, Moreira AC (2010) Discordant nadir GH after oral glucose and IGF-I levels on treated acromegaly: refining the biochemical markers of mild disease activity. Horm Metab Res 42:50–55. doi:10.1055\u002Fs-0029-1239522\nNieman LK, Biller BM, Findling JW, Newell-Price J, Savage MO, Stewart PM, Montori VM (2008) The diagnosis of Cushing’s syndrome: an endocrine society clinical practice guideline. J Clin Endocrinol Metab 93:1526–1540. doi:10.1210\u002Fjc.2008-0125\nLivak KJ, Schmittgen TD (2001) Analysis of relative gene expression data using real-time quantitative PCR and the 2(-Delta Delta C(T)) method. Methods 25:402–408. doi:10.1006\u002Fmeth.2001.1262\nKim NW, Wu F (1997) Advances in quantification and characterization of telomerase activity by the telomeric repeat amplification protocol (TRAP). Nucleic Acids Res 25:2595–2597\nFan Y, Liu Z, Fang X, Ge Z, Ge N, Jia Y, Sun P, Lou F, Björkholm M, Gruber A, Ekman P, Xu D (2005) Differential expression of full-length telomerase reverse transcriptase mRNA and telomerase activity between normal and malignant renal tissues. Clin Cancer Res 11:4331–4337. doi:10.1158\u002F1078-0432.CCR-05-0099\nOrtiz-Plata A, Tena Suck ML, López-Gómez M, Heras A, Sánchez García A (2007) Study of the telomerase hTERT fraction, PCNA and CD34 expression on pituitary adenomas. association with clinical and demographic characteristics. J Neurooncol 84:159–166. doi:10.1007\u002Fs11060-007-9365-8\nTakubo K, Izumiyama-Shimomura N, Honma N, Sawabe M, Arai T, Kato M, Oshimura M, Nakamura K-I (2002) Telomere lengths are characteristic in each human individual. 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             \u003Cjats:title>Purpose\u003C\u002Fjats:title>\n              \u003Cjats:p>Metabolic dysfunction-associated steatotic liver disease (MASLD) may have distinctive pathophysiological features in type 1 diabetes (T1D). We evaluated the independent role of blood glucose control on MASLD in T1D.\u003C\u002Fjats:p>\n            \u003C\u002Fjats:sec>\u003Cjats:sec>\n              \u003Cjats:title>Methods\u003C\u002Fjats:title>\n              \u003Cjats:p>In a cross-sectional study on 659 T1D adult patients, MASLD was assessed by the Fatty Liver Index (FLI) and the Hepatic Steatosis Index (HSI). Anthropometric, biochemical, and clinical parameters were retrieved from electronic records. Blood glucose control status was evaluated by dividing participants into subgroups according to the median value of HbA1c [7.6% (60 mmol\u002Fmol)], and this analysis was repeated excluding overweight\u002Fobese patients.\u003C\u002Fjats:p>\n            \u003C\u002Fjats:sec>\u003Cjats:sec>\n              \u003Cjats:title>Results\u003C\u002Fjats:title>\n              \u003Cjats:p>Patients with HbA1c above 7.6% (60 mmol\u002Fmol) showed significantly higher MASLD indices (HSI 38 ± 6 vs. 36 ± 5, p < 0.001; FLI 26 ± 26 vs.19 ± 19, p < 0.001), and higher proportions of MASLD identified by HSI (57 vs. 44%, p < 0.001) and FLI (14 vs. 7%, p < 0.001) than patients with HbA1c below 7.6% (60 mmol\u002Fmol). Similar results were obtained for HSI after the exclusion of overweight\u002Fobese patients. Stepwise linear regression analysis confirmed that HbA1c was independently associated with HSI (r = 0.496, p = 0.009) and FLI (r = 0.722, p = 0.007); waist circumference with HSI (r = 0.492, p < 0.001); and waist circumference (r = 0.700, p < 0.001), HDL cholesterol (r = 0.719, p < 0.001), and LDL cholesterol (r = 0.712, p < 0.001) with FLI.\u003C\u002Fjats:p>\n            \u003C\u002Fjats:sec>\u003Cjats:sec>\n              \u003Cjats:title>Conclusions\u003C\u002Fjats:title>\n              \u003Cjats:p>Blood glucose control is a main factor associated with MASLD in adults with T1D, also independently of overweight and obesity. 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R., Hart D.M., Forrest C, Baird C. Prevention of spinal osteoporosis in oophorectomized women. Lancet 2:1151, 1980.",{"doi":1580},"10.1016\u002FS0140-6736(80)92592-1",{"id":18,"text":1582,"url":18,"identifiers":1583},"Christiansen C, Christensen M.S., Transbol I. Bone mass in postmenopausal women after withdrawal of oestrogen-gestagen replacement therapy. Lancet 7; 459, 1981.",{"doi":1584},"10.1016\u002FS0140-6736(81)91848-1",{"id":18,"text":1586,"url":18,"identifiers":1587},"Aitken J.M., Hart D.M., Anderson J.B., Lindsay R., Smith D.A., Speirs CF. Osteoporosis after oophorectomy for non-malignant disease in premenopausal women. Br. Med. J. 2:235, 1973.",{"doi":1588},"10.1136\u002Fbmj.2.5860.235",{"id":18,"text":1590,"url":18,"identifiers":1591},"Eriksen E.F., Colvard D.S., Berg N.J., Graham M.L., Mann K.G., Spelsberg T.C., Riggs B.L. Evidence of oestrogen receptors in normal human osteoblast-like cells. Science 241: 84, 1988.",{"doi":1592},"10.1126\u002Fscience.3388021",{"id":18,"text":1594,"url":18,"identifiers":1595},"Stevenson J.C., Abeyasekera G., Hillyard C.J., Phang K.G., MacIntyre I., Campbell S., Young O., Towsend P.T., Whitehead M.I. Calcitonin and the calcium regulating hormones in postmenopausal women: effect of estrogens. Lancet 1: 693, 1981.",{"doi":1596},"10.1016\u002FS0140-6736(81)91973-5",{"id":18,"text":1598,"url":18,"identifiers":1599},"Civitelli R., Agnusdei D., Nardi P., Zacchei F., Avioli L.V., Gennari C. Effects of one-year treatment with estrogens on bone mass, intestinal calcium absorption and 25-hydroxy-vitamin D-1 alpha hydroxylase reserve in postmenopausal osteoporosis. Calcif. Tissue Int. 42:77, 1988.",{"doi":1600},"10.1007\u002FBF02556338",{"id":18,"text":1602,"url":18,"identifiers":1603},"Greenberg C, Kukreja S.C., Bowser E.N., Hargis G.K., Henderson W.J., Williams G.A. Effects of estradiol and progesterone on calcitonin secretion. Endocrinology 118:2594, 1986.",{},{"id":18,"text":1605,"url":18,"identifiers":1606},"Hillyard C.J., Mac Intyre I., Stevenson J.C. Relative deficiency of plasma calcitonin in normal women. Lancet 2:961, 1978.",{"doi":1607},"10.1016\u002FS0140-6736(78)90249-0",{"id":18,"text":1609,"url":18,"identifiers":1610},"Withehead M., Lange G., Young O., Campbell S., Abeyasekera G., Hillyard C.J., Mac Intyre I., Phang K.G. Interrelations of calcium regulating hormones during normal pregnancy. Br. Med. J. 282:10, 1981.",{"doi":1611},"10.1136\u002Fbmj.283.6283.10",{"id":18,"text":1613,"url":18,"identifiers":1614},"Zsely J., Szucs J., Steczek K., Szathmari M., Kollin CS., Horvath C.S., Garth M., Hollo I. Decrease of calcitonin reserve in accelerated postmenopausal osteoporosis. Horm. Metab. Res. 77:696, 1985.",{"doi":1615},"10.1055\u002Fs-2007-1013650",{"id":18,"text":1617,"url":18,"identifiers":1618},"Morimoto S., Tsiyi M., Okada Y., Owishi T., Kumahara Y. The effects of oestrogens on human calcitonin secretion after calcium infusion in elderly female subjects. Clin. Endocrinol. (Oxf.) 13:135, 1980.",{"doi":1619},"10.1111\u002Fj.1365-2265.1980.tb01034.x",{"id":18,"text":1621,"url":18,"identifiers":1622},"Isaia G.C., Campagnoli C, Mussetta M., Massobrio M., Salamano G., Gallo M., Molinatti G.M. Calcitonin and lumbar bone mineral content during oestrogen-progestogen administration in postmenopausal women. Maturitas 11:287, 1989.",{"doi":1623},"10.1016\u002F0378-5122(89)90025-X",{"id":18,"text":1625,"url":18,"identifiers":1626},"Agnusdei D., Civitelli R., Camporeale A., Gennari C. Calcitonin and estrogens. J. Endocrinol. Invest. 73:625, 1990.",{"doi":1627},"10.1007\u002FBF03349583",{"id":18,"text":1629,"url":18,"identifiers":1630},"Emmertsen K., Marquersen J., Jensen F.F., Hansen H.H. Radioimmunoassay of calcitonin in unextracted human serum: a sensitive method. Scand. J. Clin. Lab. Invest. 42:539, 1982.",{"doi":1631},"10.3109\u002F00365518209168126",{"id":18,"text":1633,"url":18,"identifiers":1634},"Reginster J.Y., Deroisy R., Albert A., Denis D., Lecart M.P., Collette J., Franchimont P. Relationship between whole plasma calcitonin secretory capacity and plasma levels of estrone in healthy women and postmenopausal osteoporosis. J. Clin. Invest. 83: 1073, 1989.",{"doi":1635},"10.1172\u002FJCI113950",{"id":18,"text":1637,"url":18,"identifiers":1638},"Lobo RA, Roy S., Shoupe D., Endres D.B., Adams J.S., Rude R.R., Singer F.R. Estrogen and progestin effects on urinary calcium and calciotropic hormones in surgically induced post-menopausal women. Horm. Metab. Res. 77:370, 1985.",{"doi":1639},"10.1055\u002Fs-2007-1013545",{"id":18,"text":1641,"url":18,"identifiers":1642},"Gallagher J.C, Riggs B.L., Jerpbak C. M., Arnaud C.D. The effect of age on serum immunoreactive parathy roid hormone in normal and osteoporotic women. J. Lab. Clin. Med. 95:373, 1980.",{},{"id":1644,"createTime":1645,"updateTime":1646,"relativeEntities":1647,"slug":1648,"properties":1649,"entityType":244,"verifyStatus":417,"verifyTime":1660,"verifyNote":419,"languages":18,"translateLanguages":18,"viewCount":19,"primaryUrl":1661,"fullTextUrl":18,"authors":1662,"publicationType":345,"publisherRelationship":1739,"citationCount":19,"citationInfo":1790,"publishDate":1792,"publishYear":398,"citationAnalyzeStatus":1573,"lastCitationAnalyze":1646,"indexDatabases":1793,"openAccess":18,"references":18,"isForceReanalyzing":400},"111c1018-2c1e-4db1-89d7-44576be2f1f9","2023-12-02T06:41:20.453+00:00","2026-08-18T06:58:12.817+00:00",[],"Effect-of-thyroxine-therapy-on-bone-metabolism-in-substituted-hypothyroid-patients-with-normal-or-suppressed-levels-of-TSH",{"abstract":1650,"title":1652,"gsPaper":1654,"references":1656,"doi":1658},{"EN":1651},"The statement that pituitary hyperthyroidism reflects peripheral hyperthyroidism is still controversial. To evaluate a possible relationship between the calcium and the thyroid metabolism, 29 women with thyroxine (T4) substituted hypothyroidism were examined. They were separated into two groups, one with normal (0.15 to 6 mU\u002Fl) and one with suppressed TSH (\u003C0.15 mU\u002Fl). All the women were judged euthyroid both by their T4 and T3 and by their clinics. The daily dose of T4 (median 0.15 mg in both groups) had been unchanged and TSH level had been stable during the previous six months. Bone mineral content (BMC) of the lumbar spine, bone mineral density (BMD) of left and right collum femoris, serum alkaline phosphatase activity (AP), serum concentration of osteocalcin (0st) and urinary excretion of hydroxyproline\u002Fcreatinine (Hpr\u002Fcrea) were similar in the two groups. Furthermore, sex- hormone-binding-globulin (SHBG) was equal in the two groups, but significantly higher than in normals (p \u003C 0.01). A significant positive correlation was found between serum 0st and Hpr\u002Fcrea (p \u003C 0.05) indicating a balanced state where bone formation equals bone resorption. AP failed to correlate to 0st and Hpr\u002Fcrea because the AP raises from both bone and liver of bone and liver metabolism whereas the two others predominantly reflect bone metabolism. SHBG, being a marker of liver metabolism, was elevated in both groups, probably because of the oral administration of T4. Our data suggest that euthyroid, T4 substituted patients have a normal calcium metabolism whether TSH levels are suppressed or not.",{"EN":1653},"Effect of thyroxine therapy on bone metabolism in substituted hypothyroid patients with normal or suppressed levels of TSH",{"VOID":1655},"[\"1321881291064010480\"]",{"VOID":1657},"Kirkegaard B., Beck K., Bregengård C., Faber J., Feldt-Rasmussen U. Thyroid stimulating hormone (TSH) in the serum as the first investigation in thyrotoxicosis. Dan. Med. Bull. 148: 897, 1986.\nMori T., Imura H., Bito S., Ikekubo K., Inoue S., Hashida S., Ishikawa E., Ogawa H. Clinical usefulness of highly sensitive enzyme-immuno-assay of TSH. Clin. Endocrinol. (Oxf.) 27: 1, 1987.\nFraser S., Smith D., Anderson J., Wilson G. Osteoporosis and fractures following thyrotoxicosis. Lancet 1: 981, 1977.\nMosekilde L., Meisen F., Bagger J.P., Myhre-Jensen O., Sorensen N.S. Bone changes in hyperthyroidism: Interrelationships between bone morphometry, thyroid function and calcium-phosphorus metabolism. Acta Endocrinol. (Copenh.) 85: 515, 1977.\nSmith D., Fraser S., Wilson G. Hyperthyroidism and calcium metabolism. Clin. Endocrinol. Metab. 2: 333, 1973.\nLinde J., Friis T. Osteoporosis in hyperthyroidism estimated by photon absorptiometry. Acta Endocrinol. (Copenh.) 91: 437, 1978.\nLukert B., Higgens J., Stoskopf M. Serum osteocalcin is increased in patients with hyperthyroidism and decreased in patients receiving glucocorticoids. J. Clin. Endocrinol. Metab. 62: 1056, 1986.\nMartinez M., Herranz L., de Pedro C., Pallardo L. Osteocalcin levels in patients with hyper- and hypothyroidism. Horm. Metab. Res. 18: 12, 1986.\nFaber J., Perrild H., Johansen J. Bone Gla Protein and Sex Hormone-Binding Globulin in nontoxic goiter: Parameters for metabolic status at the tissue level. J. Clin. Endocrinol. Metab. 70: 49, 1990.\nWenzel K. Does suppressive therapy with levothyroxine (LT4) induce tissue thyrotoxicosis. Ann. Endocrinol. 17: 172, 1988.\nRoss D., Neer R., Ridgway E., Daniels G. Subclinical hyperthyroidism and reduced bone density as a possible result of prolonged suppression of the pituitary-thyroid axis with L-thyroxine. Am. J. Med. 82: 1167, 1987.\nPaul T., Kerrigan J., Kelly A., Braverman L., Baran D. Long-term L-thyroxine therapy is associated with decreased hip bone density in premenopausal women. JAMA 259: 3137, 1988.\nAdlin E., Maurer A., Marks A., Channick B. Bone mineral density in postmenopausal women treated with thyroxine. 63rd Annual Meeting of the American Thyroid Association. Montreal Canada, 1988, T–17.\nAhmann A., Solomon B., Duncan W., Wartofsky L. Normal Bone Mineral density (BMD) in premenopausal women on suppressive doses of l-thyroxine. 62rd Annual Meeting of the American Thyroid Association. Washington D.C. 1987, T–21.\nHarvey R., McHardy K., Robins S., Taylor S., Reid I., Bewsher P. Bone collagen degradation in thyrotoxicosis and thyroxine replacement therapy measured by urinary pyridinoline and deoxypyridinoline excretion. Ann. Endocrinol. 18: 122, 1989.\nNyström E., Lundberg P., Petersen K., Bentsson C., Lindtstedt G. Evidence for slow tissue adaptation to circulating thyroxine with chronic L-thyroxine treatment. Clin. Endocrinol. (Oxf.) 31: 143, 1989.\nKrölner B., Nielsen S.P. Measurement of bone mineral content (BMC) of the lumbar spine I. Theory and application of a new two-dimensional dual-photon attenuation. Scand. J. Clin. Lab. Invest. 40: 653, 1980.\nBohr H., Schaadt O. Influence of age on bone mineral content in the femoral neck measured by dual photon absorptiometry. In: Dequeker J, Johnston C.C. (Eds.), Noninvasive bone measurement: Methodological problems. IRL Press, Oxford, 1982, p. 197.\nHyldstrup L., Clemmensen I., Jensen B., Transbøl I. Non-invasive evaluation of bone formation: measurements of serum alkaline phosphatase, whole body retention of diphosphonate and serum osteocalcin in metabolic disorders and thyroid disease. Scand. J. Clin. Lab. Invest. 48: 611, 1988.\nRibot C., Tremollieres F., Pouilles M., Louvet J.P. Bone mineral density and thyroid hormone therapy. Clin. Endocrinol. (Oxf.) 33: 143, 1990.\nKrölner B., Jørgensen J., Nielsen S.P. Spinal bone mineral content in myxedema and thyrotoxicosis. Effect of thyroid hormone and antithyroid treatment. Clin. Endocrinol. (Oxf.) 8: 439, 1983.\nGow S., Caldwell G., Toft A., Bechett G. Different hepatic responses to thyroxine replace ment in spontaneous and 131I-induced primary hypothyroidism. Clin. Endocrinol. (Oxf.) 30: 505, 1989.\nSarne D., Refetoff S., Rosenfield R., Farriaux J. Sex hormone-binding-globulin in the diagnosis of peripheral tissue resistance to thyroid hormone: The value of changes after short term triiodothyronine administration. J. Clin. Endocrinol. 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is a skeletal disease which predisposes to fragility fractures with high morbidity and economic impact, and, therefore, the goal of any osteoporosis treatment is to reduce the fracture risk. In the various forms of osteoporosis an imbalance between bone resorption and apposition is present, that generally leads to a reduction of bone mineral density and bone quality, and finally to the increased fracture risk. Nowadays, several drugs are available with a demonstrated anti-fracturative effect obtained by inhibiting bone resorption or stimulating bone formation. However, their use is not free from limitations and side effects. Importantly, to date, the available antiresorptive drugs have also an inhibiting, though to a lesser extent, effect on bone apposition and, similarly, the anabolic drugs lead to an increase also of bone resorption. Advances in our knowledge about bone biology, with molecular insights into mechanisms underlying osteoblast, osteoclast, and osteocyte activity, have led to the recognition of new potential targets and consequently to the formulation of new therapeutic agents to treat osteoporosis. New potential developments among the antiresorptive drugs include cathepsin K inhibitors and among the osteoanabolic drugs those activating the Wnt signaling pathway, such as the monoclonal antibodies against sclerostin. The novelty of these compounds is that their mechanism of action gives the exciting possibility to uncouple bone resorption and bone formation, and data available so far appear to be promising. Finally, several new therapeutic targets are under investigation in preclinical studies which could open further approaches to treat osteoporosis in the future.",{"EN":1804},"Perspectives on osteoporosis therapies",{"VOID":1806},"[]",{"VOID":1808},"NIH Consensus Development Panel on Osteoporosis Prevention, Diagnosis, and Therapy (2001) Osteoporosis prevention, diagnosis, and therapy. JAMA 285(6):785–795\nCummings SR, Melton LJ (2002) Epidemiology and outcomes of osteoporotic fractures. Lancet 359(9319):1761–1767\nIshtiaq S, Fogelman I, Hampson G (2014) Treatment of post-menopausal osteoporosis: beyond bisphosphonates. J Endocrinol Invest. doi:10.1007\u002Fs40618-014-0152-z\nLeung P, Pickarski M, Zhuo Y, Masarachia PJ, Duong LT (2011) The effects of the cathepsin K inhibitor odanacatib on osteoclastic bone resorption and vesicular trafficking. Bone 49(4):623–635. doi:10.1016\u002Fj.bone.2011.06.014\nVääräniemi J, Halleen JM, Kaarlonen K, Ylipahkala H, Alatalo SL, Andersson G, Kaija H, Vihko P, Väänänen HK (2004) Intracellular machinery for matrix degradation in bone-resorbing osteoclasts. J Bone Miner Res 19(9):1432–1440\nZerbini CA, McClung MR (2013) Odanacatib in postmenopausal women with low bone mineral density: a review of current clinical evidence. Ther Adv Musculoskelet Dis 5(4):199–209. doi:10.1177\u002F1759720X13490860\nBone HG, McClung MR, Roux C, Recker RR, Eisman JA, Verbruggen N, Hustad CM, DaSilva C, Santora AC, Ince BA (2010) Odanacatib, a cathepsin-K inhibitor forosteoporosis: a 2-year study in postmenopausal women with low bone density. J Bone Miner Res 25(5):937–947. doi:10.1359\u002Fjbmr.091035\nGauthier JY, Chauret N, Cromlish W, Desmarais S, le Duong T, Falgueyret JP, Kimmel DB, Lamontagne S, Léger S, LeRiche T, Li CS, Massé F, McKay DJ, Nicoll-Griffith DA, Oballa RM, Palmer JT, Percival MD, Riendeau D, Robichaud J, Rodan GA, Rodan SB, Seto C, Thérien M, Truong VL, Venuti MC, Wesolowski G, Young RN, Zamboni R, Black WC (2008) The discovery of odanacatib (MK-0822), a selective inhibitor of cathepsin K. Bioorg Med Chem Lett 18(3):923–928. doi:10.1016\u002Fj.bmcl.2007.12.047\nMasarachia PJ, Pennypacker BL, Pickarski M, Scott KR, Wesolowski GA, Smith SY, Samadfam R, Goetzmann JE, Scott BB, Kimmel DB, le Duong T (2012) Odanacatib reduces bone turnover and increases bone mass in the lumbar spine of skeletally mature ovariectomized rhesus monkeys. J Bone Miner Res 27(3):509–523. doi:10.1002\u002Fjbmr.1475\nCusick T, Chen CM, Pennypacker BL, Pickarski M, Kimmel DB, Scott BB, le Duong T (2012) Odanacatib treatment increases hip bone mass and cortical thickness by preserving endocortical bone formation and stimulating periosteal bone formation in the ovariectomized adult rhesus monkey. J Bone Miner Res 27(3):524–537. doi:10.1002\u002Fjbmr.1477\nStoch SA, Zajic S, Stone J, Miller DL, Van Dyck K, Gutierrez MJ, De Decker M, Liu L, Liu Q, Scott BB, Panebianco D, Jin B, Duong LT, Gottesdiener K, Wagner JA (2009) Effect of the cathepsin K inhibitor odanacatib on bone resorption biomarkers in healthy postmenopausal women: two double-blind, randomized, placebo-controlled phase I studies. Clin Pharmacol Ther 86(2):175–182. doi:10.1038\u002Fclpt.2009.60\nEisman JA, Bone HG, Hosking DJ, McClung MR, Reid IR, Rizzoli R, Resch H, Verbruggen N, Hustad CM, DaSilva C, Petrovic R, Santora AC, Ince BA, Lombardi A (2011) Odanacatib in the treatment of postmenopausal women with low bone mineral density: 3-year continued therapy and resolution of effect. J Bone Miner Res 26(2):242–251. doi:10.1002\u002Fjbmr.212\nLangdahl B, Binkley N, Bone H, Gilchrist N, Resch H, Rodriguez Portales J, Denker A, Lombardi A, Le Bailly De TC, Dasilva C, Rosenberg E, Leung A (2012) Odanacatib in the treatment of postmenopausal women with low bone mineral density: 5 years of continued therapy in a phase 2 study. J Bone Miner Res 27(11):2251–2258. doi:10.1002\u002Fjbmr.1695\nBrixen K, Chapurlat R, Cheung AM, Keaveny TM, Fuerst T, Engelke K, Recker R, Dardzinski B, Verbruggen N, Ather S, Rosenberg E, de Papp AE (2013) Bone density, turnover, and estimated strength in postmenopausal women treated with odanacatib: a randomized trial. J Clin Endocrinol Metab 98(2):571–580. doi:10.1210\u002Fjc.2012-2972\nEngelke K, Fuerst T, Dardzinski B, Kornak J, Ather S, Genant HK, de Papp A (2014) Odanacatib treatment affects trabecular and cortical bone in the femur of postmenopausal women—results of a 2-year placebo-controlled trial. J Bone Miner Res. doi:10.1002\u002Fjbmr.2292\nFeng S, Luo Z, Liu D (2014) Efficacy and safety of odanacatib treatment for patients with osteoporosis: a meta-analysis. J Bone Miner Metab. doi:10.1007\u002Fs00774-014-0609-3\nGajic-Veljanoski O, Tomlinson G, Srighanthan J, Adachi JD, Josse R, Brown JP, Cheung AM (2014) Effect of odanacatib on BMD and fractures: estimates from Bayesian Univariate and bivariate meta-analyses. J Clin Endocrinol Metab 99(9):3070–3079. doi:10.1210\u002Fjc.2014-1162\nEastell R, Nagase S, Ohyama M, Small M, Sawyer J, Boonen S, Spector T, Kuwayama T, Deacon S (2011) Safety and efficacy of the cathepsin K inhibitor ONO-5334 in postmenopausal osteoporosis: the ocean study. J Bone Miner Res 26(6):1303–1312. doi:10.1002\u002Fjbmr.341\nEastell R, Nagase S, Small M, Boonen S, Spector T, Ohyama M, Kuwayama T, Deacon S (2014) Effect of ONO-5334 on bone mineral density and biochemical markers of bone turnover in postmenopausal osteoporosis: 2-year results from the ocean study. J Bone Miner Res 29(2):458–466. doi:10.1002\u002Fjbmr.2047\nEngelke K, Nagase S, Fuerst T, Small M, Kuwayama T, Deacon S, Eastell R, Genant HK (2014) The effect of the cathepsin K inhibitor ONO-5334 on trabecular and cortical bone in postmenopausal osteoporosis: the ocean study. J Bone Miner Res 29(3):629–638. doi:10.1002\u002Fjbmr.2080\nNagase S, Ohyama M, Hashimoto Y, Small M, Sharpe J, Manako J, Kuwayama T, Deacon S (2014) Bone turnover markers and pharmacokinetics of a new sustained-release formulation of the cathepsin K inhibitor, ONO-5334, in healthy post-menopausal women. J Bone Miner Metab. doi:10.1007\u002Fs00774-013-0558-2\nTanaka M, Hashimoto Y, Sekiya N, Honda N, Deacon S, Yamamoto M (2014) Effects of novel cathepsin K inhibitor ONO-5334 on bone resorption markers: a study of four sustained release formulations with different pharmacokinetic patterns. J Bone Miner Metab 32(4):447–454. doi:10.1007\u002Fs00774-013-0517-y\nSoriano P, Montgomery C, Geske R, Bradley A (1991) Targeted disruption of the c-src proto-oncogene leads to osteopetrosis in mice. Cell 64(4):693–702\nMarzia M, Sims NA, Voit S, Migliaccio S, Taranta A, Bernardini S, Faraggiana T, Yoneda T, Mundy GR, Boyce BF, Baron R, Teti A (2000) Decreased c-Src expression enhances osteoblast differentiation and bone formation. J Cell Biol 151(2):311–320\nde Vries TJ, Mullender MG, van Duin MA, Semeins CM, James N, Green TP, Everts V, Klein-Nulend J (2009) The Src inhibitor AZD0530 reversibly inhibits the formation and activity of human osteoclasts. Mol Cancer Res 7(4):476–488. doi:10.1158\u002F1541-7786.MCR-08-0219\nHannon RA, Clack G, Rimmer M, Swaisland A, Lockton JA, Finkelman RD, Eastell R (2010) Effects of the Src kinase inhibitor saracatinib (AZD0530) on bone turnover in healthy men: a randomized, double-blind, placebo-controlled, multiple-ascending-dose phase I trial. J Bone Miner Res 25(3):463–471. doi:10.1359\u002Fjbmr.090830\nFitzpatrick LA, Dabrowski CE, Cicconetti G, Gordon DN, Papapoulos S, Bone HG 3rd, Bilezikian JP (2011) The effects of ronacaleret, a calcium-sensing receptor antagonist, on bone mineral density and biochemical markers of bone turnover in postmenopausal women with low bone mineral density. J Clin Endocrinol Metab 96(8):2441–2449. doi:10.1210\u002Fjc.2010-2855\nHalse J, Greenspan S, Cosman F, Ellis G, Santora A, Leung A, Heyden N, Samanta S, Doleckyj S, Rosenberg E, Denker AE (2014) A phase 2, randomized, placebo-controlled, dose-ranging study of the calcium-sensing receptor antagonist MK-5442 in the treatment of postmenopausal women with osteoporosis. J Clin Endocrinol Metab 99(11):E2207–E2215. doi:10.1210\u002Fjc.2013-4009\nRochefort GY (2014) The osteocyte as a therapeutic target in the treatment of osteoporosis. Ther Adv Musculoskelet Dis 6(3):79–91. doi:10.1177\u002F1759720X14523500\nPadhi D, Jang G, Stouch B, Fang L, Posvar E (2011) Single-dose, placebo-controlled, randomized study of AMG 785, a sclerostin monoclonal antibody. J Bone Miner Res 26(1):19–26. doi:10.1002\u002Fjbmr.173\nMcClung MR, Grauer A, Boonen S, Bolognese MA, Brown JP, Diez-Perez A, Langdahl BL, Reginster JY, Zanchetta JR, Wasserman SM, Katz L, Maddox J, Yang YC, Libanati C, Bone HG (2014) Romosozumab in postmenopausal women with low bone mineral density. N Engl J Med 370(5):412–420. doi:10.1056\u002FNEJMoa1305224\nMcColm J, Hu L, Womack T, Tang CC, Chiang AY (2014) Single- and multiple-dose randomized studies of blosozumab, a monoclonal antibody against sclerostin, in healthy postmenopausal women. J Bone Miner Res 29(4):935–943. doi:10.1002\u002Fjbmr.2092\nRecker R, Benson C, Matsumoto T, Bolognese M, Robins D, Alam J, Chiang AY, Hu L, Krege JH, Sowa H, Mitlak B, Myers S (2014) A randomized, double-blind phase 2 clinical trial of blosozumab, a sclerostin antibody, in postmenopausal women with low bone mineral density. J Bone Miner Res. doi:10.1002\u002Fjbmr.2351\nEvenepoel P, D’Haese P, Brandenburg V (2014) Romosozumab in postmenopausal women with osteopenia. N Engl J Med 370(17):1664. doi:10.1056\u002FNEJMc1402396#SA1\nvan Lierop AH, Hamdy NA, Hamersma H, van Bezooijen RL, Power J, Loveridge N, Papapoulos SE (2011) Patients with sclerosteosis and disease carriers: human models of the effect of sclerostin on bone turnover. J Bone Miner Res 26(12):2804–2811. doi:10.1002\u002Fjbmr.474\nvan Lierop AH, Hamdy NA, van Egmond ME, Bakker E, Dikkers FG, Papapoulos SE (2013) Van Buchem disease: clinical, biochemical, and densitometric features of patients and disease carriers. J Bone Miner Res 28(4):848–854. doi:10.1002\u002Fjbmr.1794\nBalemans W, Ebeling M, Patel N, Van Hul E, Olson P, Dioszegi M, Lacza C, Wuyts W, Van Den Ende J, Willems P, Paes-Alves AF, Hill S, Bueno M, Ramos FJ, Tacconi P, Dikkers FG, Stratakis C, Lindpaintner K, Vickery B, Foernzler D, Van Hul W (2011) Increased bone density in sclerosteosis is due to the deficiency of a novel secreted protein (SOST). Hum Mol Genet 10(5):537–543\nLoots GG, Kneissel M, Keller H, Baptist M, Chang J, Collette NM, Ovcharenko D, Plajzer-Frick I, Rubin EM (2005) Genomic deletion of a long-range bone enhancer mis-regulates sclerostin in Van Buchem disease. Genome Res 15(7):928–935\nGardner JC, van Bezooijen RL, Mervis B, Hamdy NA, Löwik CW, Hamersma H, Beighton P, Papapoulos SE (2005) Bone mineral density in sclerosteosis; affected individuals and gene carriers. J Clin Endocrinol Metab 90(12):6392–6395\nMorvan F, Boulukos K, Clément-Lacroix P, Roman SR, Suc-Royer I, Vayssière B, Ammann P, Martin P, Pinho S, Pognonec P, Mollat P, Niehrs C, Baron R, Rawadi G (2006) Deletion of a single allele of the Dkk1 gene leads to an increase in bone formation and bone mass. J Bone Miner Res 21(6):934–945\nLi J, Sarosi I, Cattley RC, Pretorius J, Asuncion F, Grisanti M, Morony S, Adamu S, Geng Z, Qiu W, Kostenuik P, Lacey DL, Simonet WS, Bolon B, Qian X, Shalhoub V, Ominsky MS, Zhu KH, Li X, Richards WG (2006) Dkk1-mediated inhibition of Wnt signaling in bone results in osteopenia. Bone 39(4):754–766\nLi X, Grisanti M, Fan W, Asuncion FJ, Tan HL, Dwyer D, Han CY, Yu L, Lee J, Lee E, Barrero M, Kurimoto P, Niu QT, Geng Z, Winters A, Horan T, Steavenson S, Jacobsen F, Chen Q, Haldankar R, Lavallee J, Tipton B, Daris M, Sheng J, Lu HS, Daris K, Deshpande R, Valente EG, Salimi-Moosavi H, Kostenuik PJ, Li J, Liu M, Li C, Lacey DL, Simonet WS, Ke HZ, Babij P, Stolina M, Ominsky MS, Richards WG (2011) Dickkopf-1 regulates bone formation in young growing rodents and upon traumatic injury. J Bone Miner Res 26(11):2610–2621. doi:10.1002\u002Fjbmr.472\nGlantschnig H, Scott K, Hampton R, Wei N, McCracken P, Nantermet P, Zhao JZ, Vitelli S, Huang L, Haytko P, Lu P, Fisher JE, Sandhu P, Cook J, Williams D, Strohl W, Flores O, Kimmel D, Wang F, An Z (2011) A rate-limiting role for Dickkopf-1 in bone formation and the remediation of bone loss in mouse and primate models of postmenopausal osteoporosis by an experimental therapeutic antibody. 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In the patients with PES and hyperprolactinemia, the PRL response to TRH was significantly lower than in the controls and the patients with PES and normal PRL, which suggests there is impaired PRL synthesis and release in cases of PES with hyperpro-lactinemia. The TSH response to domperidone was significantly elevated in patients with PES and either normal or elevated PRL, as in patients with prolactinoma. The PRL response to domperidone was significantly reduced in patients with PES and hyperprolactinemia as in patients with prolactinoma. These results suggest that in PES as in prolactinoma the inhibiting dopaminergic tone is increased on the thyrotropic cells and reduced on the lactotropic cells in PES with elevated PRL and that some patients with PES might bear a microprolactinoma in the bottom of the sella which remained undetected by the CT scan.",{"EN":2112},"TSH and prolactin responses to thyrotropin releasing hormone (TRH) and domperidone in patients with empty sella syndrome",{"VOID":2114},"[\"16942389445878933195\"]",{"VOID":2116},"10.1007\u002FBF03347865","2024-05-04T13:28:00.875+00:00","https:\u002F\u002Flink.springer.com\u002Farticle\u002F10.1007\u002FBF03347865",[2120,2144,2164,2184],{"id":2121,"sortIndex":19,"researcher":18,"roles":2122,"affiliations":2123,"properties":2141,"displayName":2143,"givenName":18,"familyName":18},"9ea5bc31-b1fd-4ca9-a88c-4eb62c1cf924",[252],[2124,2132],{"id":2125,"sortIndex":19,"affiliation":2126,"properties":18},"52b94313-848b-4350-95dd-791ee8c8c5aa",{"id":2125,"createTime":18,"updateTime":18,"relativeEntities":2127,"slug":18,"properties":2128,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2131,"statistic":18},[],{"title":2129},{"VI":2130},"Service d’Endocrinologie-Diabétologie-Nutrition, Hôpital Jean Verdier, Bondy Cedex, France",[],{"id":2133,"sortIndex":267,"affiliation":2134,"properties":2140},"9f32f868-82c0-4691-9128-5a4ca700a1f4",{"id":2133,"createTime":18,"updateTime":18,"relativeEntities":2135,"slug":18,"properties":2136,"entityType":18,"verifyStatus":18,"verifyTime":18,"verifyNote":18,"languages":18,"translateLanguages":18,"viewCount":18,"url":18,"parentIds":2139,"statistic":18},[],{"title":2137},{"VI":2138},"Laboratoire de Pharmacologie Clinique et Expérimentale, Hôpital Avicenne, Bobigny, France",[],{},{"title":2142},{"VI":2143},"P. 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