METABOLIZAM KOSTI U TOKU PRIMENE SUPSTITUCIONE TERAPIJE PRIMARNOG HIPOTIROIDIZMA

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1 Med Preg12009; LXII (9-10): Novi Sad: septembar-oktobar. 407 Klinicki centar Vojvodine Novi Sad Klinika za endokrinologiju, dijabetes i bolesti metabolizma' Medicinski fakultet Novi Sad Institut za laboratorijsku medicine" Originalni naucni rad Original study UDK : : /MPNS P METABOLIZAM KOSTI U TOKU PRIMENE SUPSTITUCIONE TERAPIJE PRIMARNOG HIPOTIROIDIZMA BONE METHABOLISMDURING SUBSTITUTION THERAPY OF PRIMARYHYPOTHYROIDISM Radoslav PEJIN I, Nikola CURIC:!, Branka KOVACEV-ZAVISIc l i Ljiljana TODOROVIC-DILAS I Sazetak - Istazivanje je imalo za cilj da proceni efekte fizioloskih doza supstitucione terapije I-tiroksinom na metabolizam kosti kod bolesnika obolelih od primarnog hipotiroidizma. U studijskoj grupi od 30 bolesnika individualnim doziranjem leka postignuto je eutireoidno stanje, koje je potvrdeno klinicki i laboratorijski. Merenja parametara metabolizma kosti i kalcijuma kao i tiroidnog statusa, koje predstavljaju osteokalcin, alkalna fosfataza, C-terminalni telopeptid kolagena, parathormon, ukupni i jonizovani kalcijum, fosfor, trijodtironin, tiroksin, tirostirnulisuci horrnon), vrsena su u dva navrata, nakon postavljanja dijagnoze (hipotiroidno stanje) i po uspostavljanju eutiroidnog stanja. U odnosu na hipotireoidno stanje bolesnika metabolizam kosti u eutireoidnom stanju bolesnika pokazivao je statisticki znacajno vise vrednosti parametara kostane formacije i resorpcije (osteokalcin: p=o, i C terminalni telopeptid kolagena: p=o,002648). Porast ovih parametara pokazivao medusobno visoku korelaciju, tj. odvijao se sinhrono i predstav Ija prognosticki argument protiv kostanog gubitka u toku fizioloske supstitucije tiroidnim hormonima. Nivoi jonizovanog kalcijuma su takode pokazivali signifikantno vise vrednosti u eutiroidnom stanju (p=o,02) dok se serumski nivoi parathormona nisu signifikantno razlikovali pre i toku terapije (p=0,24). Nivoi tiroidnih hormona su pokazali znacajne korelacije sa nivoima parametara metabolizma kosti pre terapije. Ipak, neophodne su dugotrajnije studije da bi se potvrdila pretpostavka moguceg ostecujuceg delovanja terapije I-tiroksinom na kostani sistem. Kljucne reei: Kosti + metabolizam; Hipotireoidizam: L-Tiroksin + terapijska primena; Tireoidni hormoni; Resorpcija kosti Uvod Tiroidni hormoni ubrzavaju metabolizam prakticno svih tkiva u ljudskom organizmu. Povisene koncentracije tiroidnih hormona u hipertiroidizmu u odnosu na metabolizam kosti dovode do ubrzanja kostanog turnover-a i skracivanja perioda remodelovanja kosti sto rezultira pojavom osteoporoze i povisenim rizikom od fraktura. Stanje hipotiroidizma nasuprot prethodnom, povezano je sa smanjenim kostanim turnover-om i osteosklerozom [1,2] koji se cesto koriguju terapijom tireoidnim hormonima [3]. Pojedine ranije studije sugerisu razlike izmedu pacijenta na tiroksinskoj terapij i i kontrolne grupe zdravih po pitanju parametara metabolizma kosti kao i mogucnost povecanog gubitka kostanog tkiva u toku dugotrajne supstitucije l-tiroksinom [4,5]. Za preparate l-tiroksina koji se koriste u lecenju tiroidnih karcinoma u cilju suprimiranja vrednosti tirostimulisuceg hormona velike meta-analize su pokazale da imaju stetni efekat na kostanu homeostazu, narocito kod zena u postmenopauzi [6]. Tiroidni hormoni imaju uzan dijapazon toksicno-terapijskog kolicnika. Nasuprot pretpostavci da lecenje njima treba da bude odlucno, istrazivanja u pojedinim studijama izvedenim na velikim populacijama [7,8], kao i lecenje bolesnika u opstoj i specijalistickoj praksi [9], pokazali su sledece rezultate: oko jedne petine bolesnika sa hipotiroidizmom uzima nedovoljnu dozu l-tiroksina, a petina posmatranih bolesnika prima ekscesivne doze leka (predoziranost). U toku razvoja bolesti primarnog hipotiroidizma dolazi, pored ostecenog i smanjenog stvaranja tiroidnih hormona, i do poremecaja sinteze serumskog kalcitonina koji produkuju Cvcelijc stitaste zlezde i koji je prirodni antiresorber, a cija se suplementacija rutinski ne sprovodi. Body i saradnici [10] su zapazili smanjene vrednosti (bazalnog i nakon stimulacije kalcijumom) nivoa kalcitonma u serumu obolelih od primarnog hipotiroidizma u poredenju sa kontrolnom grupom. U ovom istrazivanju imali smo za cilj da procenimo uticaj fizioloskih doza l-tiroksina na kostani metabolizam obolelih od primarnog hipotiroidizma u vremenskom periodu od nekoliko meseci, kao i potencijalni rizik neadekvatnog doziranja leka, narocito u grupama bolesnika koji imaju jos neki od faktora rizika za ostecenje kostanog sistema. Materijal i metode Istrazivanje je sprovedeno na uzorku od 30 novootkrivenih bolesnika sa primarnim hipotiroidizmom. Sva planirana ispitivanja su sprovedena pri postavljanju dijagnoze (prva grupa) i nakon postizanja pune supstitucione doze tiroidnim hormonima (druga grupa). Kriterijumi za ukljucivanje u studiju bili su: - klinicki i laboratorijski jasno ispoljeni znaci hipotiroidizma; - nepostojanje drugih porernecaja, hronicnih oboljenja i stanja koja mogu da uticu na metabolizam kosti (oboljenja bubrega i digestivnog sistema, oboljenja kostanog sistema, maligne bolesti, alkoholizam); Adresa autora: Asist. mr sc. med. Radoslav Pejin, Klinika za endokrinologiju, dijabetes i bolesti metabolizma, Novi Sad. Hajduk Veljkova )-7

2 408 Pejin R, i sar. Metabolizam kosti i primarni hipotioidizam Skracenice ALP - alkalna fosfataza u serumu Ca - ukupni kalcijum u serumu Ca J - jonizovani Ca u serumu CL - C teminalni peptid kolagena I-CL - C-terminalni telopeptid kolagena tipa I (~-crosslaps) OC - osteokalcin P - fosfor u serumu PTH - parathormon T3 - trijodtironin T4 - tetrajodtironin - tiroksin TSH - tirostimulisuci hormon - odsusustvo terapije bolesnika svim lekovima koji bi mogli da uticu na metabolizam kosti. Uzorak je cinilo 30 bolesnika (2 muskarca i 28 zena). ~od svih bolesnika je postignuto stanje eutiroze pnrnenom supstitucione terapije l-tiroksinom. Te~in "';1 toku terapije" odnosi se na vreme postiz.an~a ~utlroidnog. stanja fizioloskorn supstitucijom tiroidnim hormonima, Ovaj termin je odabran zbog dozivotne administracije tiroidnih hormona kod?~oleli~ o~ pri!?a~nog hipotiroidizma. Srednja duzma tr.ajanja lecenja kod bolesnika iznosila je 6,13 meseci sa standardnom devijacijom od 3,45 meseci lecenja, Pro~ecn~ primenjena doza leka iznosila je 97,90 ug l-tiroksina sa standardnom devijacijom od 23,69Ilg. K~ntrolnagrupa nije postojala iz etickih razloga. S,?bzlro.~ da se radilo 0 longitudinalnoj prospektivnoj StUdIJI, grupa ispitivanih bolesnika predstavljala je sarna sebi kontrolnu grupu. U svrhu potvrde radne hipoteze i realizacije zadataka istrazivanja, sprovedeno je odredivanje osetljivih parametara formiranja kosti (alkalna fosfataza-alp i osteokalcin-oc) i razgradnje kosti (C-terminalni telopeptid kolagena tipa I - I-CL, f3-crosslaps) zajedno sa vrednostima tiroidnih hormona (trijodtironina-t3, tiroksina-t4), nivoima serumskog tirostimulisuceg hormona (TSH), parathormona (PT~), ka.o i nekih.biohe!l1ijskih pokazatelja.. Vadenje krvi za analize svih parametara vrseno Je u dva navrata: prvo vadenje krvi je uradeno po ukljucivanju bolesnika u studiju, tj. u hipotiroidnom stanju (pre ~vo~enja s.up~titucione t~rapije), a drugo na~?n postizanja eutiroidnog stanja (puna supstitucija). Odredene su vrednosti T3, T4 i TSH u krvi radioimunoesejom (RIA) i imunoreaktivnim modifikovanimesejom (IRMA). Odredene su vrednosti kalcijuma (Ca) i fosfora (P).u krvi standardnim biohemijskim metodama, a jonizovani kalcijum (Cal) potenciometrijskom metodom. Od~edeni su seru.mski nivoi C-terminalnog telopeptida kolagena tipa 1 (f3-crosslaps) i osteokalcma metodama imunoeseja, a nivoi serumskog PTH elektrohemiluminiscentnom metodom. Odredeni su serumski nivoi ALP, y-glutamiltranspeptidaza i kreatinina standardnim biohemijskim metodama. Rezultati. U.T~b~li 1 prikazan je uticaj adekvatne tarapije hipotiroidizma na kostanu metabolicku aktivnost. Izme~.u srednj ih. vrednosti skupova koje daje promenljlv~ T3 pre I u toku terapije postoje signifikantne razlike. Terapija dovodi do statisticki znacajnog porasta promenljive T3 kod bolesnika (p = 0,00013). Izrazen relativno, ovaj porast iznosi u proseku oko 65%. Tabela 1. Uticaj adekvatne terapije hipotiroidizma na kostanu rnetabolicku aktivnost Table 1. Influence ofl-thyroxine therapy on the bone metabolism in hypothyroid patients Parametar t-test za parne Parameter vrednosti/t-testfor even values Terapija x SD t vrednost p Therapy t-value T3 Pre/Before 1, , ,2796 0, (n mol/i) U toku/during 2, ,51728 T4 Pre/Before 54, , ,5710 0, (n molll) U toku/ During 178, TSH Pre/Before 57, ,0403 0, (mull) U toku/during 2, PTII Pre/Before 34, ,88437 Ll8187 0, (pg/ml) U toku/ During 30, OC Pre/Before 16, , , , (ng/ml) U tokulduring 27, ,19416 CL Pre/Before 219, , , (pg/rnl). UtokulDuring Ca++ Pre/Before Ll , , , (mmol/l) U toku/ During , TerapUa dovodi do statisticki znacajnog porasta promcnljivc T4 kod bolesnika (p=o,ooo). Izrazen relativno, ovaj porast iznosi u proseku oko 227%. Pre terapije srednja vrednost promenlj ive TSH nalazila se iznad gornje granice intervala normalnih vrednosti. U toku terapije, srednja vrednost prom enljive TSH svedenaje u interval normalnih vrednosti. Pre terapije i u toku terapije, srednja vrednost promenljive PTH nalazila se u intervalu normalnih vrednosti. Izrnedu srednjih vrednosti skupova koje daje promenljiva PTH pre i u toku terapije ne postoje signifikantne razlike, tj. terapija ne dovodi do statisticki znacajne promene promenljive PTH kod bolesnika (p = 0,247). promenljiva OC pre i u toku terapije postoje signifikantne razlike. Terapija dovodi do statisticki znacajnog porasta promenljive OC kod bolesnika (p = 0,000024). Izrazen relativno, ovaj porast iznosi u proseku oko 68%. Izmedu srednj ih vrednosti skupova koje daje promenljiva C-terminalni telopeptid kolagena-cl, pre i u toku terapije postoje signifikantne razlike. Terapija dovodi do statisticki znacajnog porasta promenljive CL kod bolesnika (p = 0,0026). Izrazen relativno,ovaj porast iznosi u proseku oko 58%.

3 Med Preg12009; LXII (9-10): Novi Sad: septembar-oktobar. 409 promenljiva jonizovani kalcijum, pre i u toku terapije postoje signifikantne razlike (p = 0,020). Terapija dovodi do statisticki znacajnog porasta promenljive Ca 1 kod bolesnika. Izrazen relativno, ovaj porast iznosi u proseku oko 3,4%. promenljiva ukupna alkalna fosfataza, pre i u toku terapije ne postoje signifikantne razlike. Terapija ne dovodi do statisticki znacajnog porasta promenljive ALP kod bolesnika (p = 0,33). U Tabeli 2 date su vrednosti koeficijenata linearne korelacije izmedu ispitivanih promenljivih pre terapije. Pre terapije isticu se funkcionalni, jaki i umereni linearni odnosi promenljivih T3 sa T4, T3 sa TSH, T3 sa OC, T3 sa CL, T4 sa TSH, T4 sa OC, OC sa CL, OC sa ALP. Tabela 2. Korelacije izmedu vrednosti ispitivanih promenljivih pre terapije Table 2. Correlation between parameters ofthyroid status and bone metabolism before therapy T3 T4 TSH PTH oc CL ALP Ca Cal P 13 0,93 0,77 0,20 0,67 0,60 0,48-0,22 0,55-0,21 T4 0,93 0,79 0,10 0,61 0,58 0,48-0,25 0,49-0,26 TSH -0,77-0,79-0,27-0,51-0,58-0,46 0,12-0,44 0,23 PTH 0,20 0,10-0,27 0,18 0,23 0,34 0,14 0,23 0,11 OC 0,67 0,61-0,51 0,18 0,82 0,61 0,01 0,36-0,09 CL 0,60 0,58-0,58 0,23 0,82 0,57-0,03 0,33-0,05 ALP 0,48 0,48-0,46 0,34 0,61 0,57-0,08 0,51 0,11 cs: -0,22-0,25 0,12-0,14 0,01-0,03-0,08-0,09 0,31 CaJ 0,55 0,49-0,44 0,23 0,36 0,33 0,51-0,09 0,25 P -0,21-0,26 0,23 0,11 0,09-0,05 0,11 0,31 0,25 U toku terapije evidentiran je sarno jedan jak linearan odnos, i to izmedu promenljivih OC i CL. U slucaju odnosa OC i CL znacajno je napomenuti da je koeficijent korelacije ostao skoro identican (Tabela 3). Tabela 3. Korelacije izmedu vrednosti ispitivanih promenljivih u toku terapije Table 3. Correlation between parameters of thyroid status and bone metabolism during therapy TSH PTH oc CL ALP Ca Cal P T3 0,42-0,37-0,43-0 0,04-0,02 0,19-0,09 0, ,42-0,51-0,16-0,09 0,09-0,26 0,36 0,03-0,04 TSH -0,37-0,51 0,04-0,16-0,28 0,02-0,31 0,03-0,13 PTH -0,43-0,16 0,04-0,13-0,24-0,06-0,19-0,01-0,33 OC -0-0,09-0,16-0,13 0,81 0,38 0,2 0,28 0,5 CL 0,04 0,09-0,28-0,24 0,81 0,2 0,18 0,23 0,46 ALP -0,02-0,26 0,02-0,06 0,38 0,2 0,18 0,09 0,17 Ca~- 1,19 0,36-0,31-0,19 0,2 0,18 0,18 0,43 0,38 Cal -0,09 0,03 0,03-0,01 0,28 0,23 0,09 0,43 0,56 P 0,12-0,04-0,13-0,33 0,5 0,46 0,17 0,38 0,56 Uticaj adekvatne terapije hipotiroidizma na kostanu metabolicku aktivnost Serumske vrednosti tiroksina (T4) pokazale su statisticki znacajan porast u toku terapije. Osamnaest bolesnika je imalo vrednosti serumskog T4 iznad maksimuma intervala normalnih vrednosti, sto je u skladu sa istrazivanjirna Langdahla i saradnika [11]. Nivoi serumskog PTH su se pre i u toku terapije nalazili u intervalima normalnih vrednosti. Statisticki znacajna razlika izmedu nivoa PTH pre i u toku terapije nije pronadena, sto je u skladu sa ranijim istrazivanjima [11-13]. Fraser i saradnici [14] su pronasli relativno vise vrednosti PTH kod hipotiroidnih bolesnika u odnosu na eutiroidne kontrole, a nize vrednosti PTH kod hipertiroidnih bolesnika i bolesnika na supstitucijskoj terapiji l-tiroksinorn u odnosu na kontrolnu grupu. Nivoi osteokalcina u serumu bili su pre terapije signifikantno nizi u odnosu na stanje eutiroze (u toku terapije) sto je u skladu sa ranijim istrazivanjima [15-18]. Izrnedu srednjih vrednosti serumskog C-telopeptida kolagena tipa I (B-crosslaps) pre i u toku terapije postoji signifikantna razlika. Terapija dovodi do statisticki znacajnog porasta nivoa crosslaps-a u ispitivanoj grupi bolesnika. Slicne nalaze po ovom pitanju nalaze Nakamura [19] i Mejer [20] ispitujuci ukrstene veze kolagena i crosslaps-e. Koeficijent linearne korelacije u ispitivanoj grupi oznacava slabu vezu izmedu vrednosti osteokalcina i crosslaps-a pre i u toku terapije, te ukazuje da vrednosti u toku terapije u vecem obimu zavise od primenjenog lecenja. Za Cal postoje signifikantne razlike izmedu srednjih vrednosti skupova pre i u toku terapije. Stall i saradnici [21] nisu pronasli statisticki znacajnu razliku izmedu nivoa jonizovanog kalcijuma kod bolesnika na supstitucionoj terapiji tiroksinom sa normalnim i suprimiranim vrednostima TSH u odnosu na kontrolnu grupu zdravih za razliku od drugih autora [22]. Nalaz signifikantne razlike u nivoima jonizovanog kalcijuma ispitivane grupe pre i u toku terapije moze da ukaze na ubrzanje kostanog rnetabolizma u toku supstitucione terapije primarnog hipotiroidizma. Izrnedu srednjih vrednosti ALP pre i u toku terapije ne postoje signifikantne razlike. Meier pronalazi signifikantan porast serumske ALP u toku supstitucione terapije supklinickog hipotiroidizma [20]. Sabancu i saradnici [13] ne pronalaze statisticki znacajne razlike serumske ALP izmedu hipotiroidnih bolesnika, bolesnika na fizioloskoj supstituciji tiroidnim hormonima i eutiroidne kontrolne grupe. Ukupni korelacioni odnosi ispitivanih parametara pre i u toku terapije nisu pokazali identicne odnose. Izrazena korelacija pre terapije uocava se izmedu parametara serumskih T3 i T4 sa nivoima osteokalcina i crosslaps-a. Niza korelacija ovih parametara primecuje se u odnosu na nivoe serumske ALP. Nakon terapije uticaj nivoa tiroidnih hormona (T3 i T4), kao i TSH, na parametre kostanog metabolizma se gubi, tj. ne pokazuje visoku korelaciju. Sabancu i saradnici nalaze u svojoj studiji korelaciju izmedu nivoa tiroidnih hormona i parametara metabolizma kosti, ukljucujuci i nivoe ALP [13]. Engler i saradnici [23] pronalaze visoku korelaciju serumskih nivoa T3 i crosslaps-ti kod bolesnika sa serumskim nivoom TSH nizirn od normale, dok u grupi eutireoidnih taj efekat nije zapazen. Guo i saradnici [24] nalaze signifikantno

4 410 Pejin R, i sar. Metabolizam kosti i primarni hipotioidizam negativnu korelaciju izrnedu nivoa serumskog TSH i parametara metabolizma kosti pre terapije. Drugi autori pronalaze vezu izmedu nivoa serumskih i slobodnih tiroidnih hormona sa nivoom osteokalcina u hipotiroidizmu [18, 25]. Gam i saradnici [26], kao i De Rosa [27] imaju rezultate slicne nasim u toku lecenja hipotiroidizma supstitucionom terapijom tiroidnim hormonima. Foscolo [17] pronalazi pozitivnu koleraciju izmedu nivoa slobodnih tiroidnih hormona i parametra metabolizma kosti i kod hipotiroidnih i kod eutiroidnih ispitanika, ali bez egzogenog uticaja terapije l-tiroksinom. U drugim studijama [13] nivoi tiroidnih hormona su bili u korelaciji sa nivoima parametara kostanog metabolizma u toku terapije, ali svi bolesnici u ovoj studiji primali su istu dozu l-tiroksina. Cini se, da se zbog razlicite doze datog leka, po kilogramu telesne mase, gube izrazeni korelacioni odnosi izmedu serumskih nivoa tiroidnih hormona i parametara metabolizma kosti u toku terapije. Zapazeno je da je koeficijent korelacije osteokalcina i crosslaps-a u toku terapije ostao skoro identican onom pre terapije, sto ukazuje da je suspstituciona terapija 1 tiroksinom ova dva parametra menjala u istoj proporciji. Ovi podaci ukazuju na sinhronost kostanog formiranja i razgradnje kod bolesnika na fizioloskim dozama supstitucije tiroidnim hormonima. Rezultate 0 sinhronoj pojavi rasta parametara kostane formacije i degradacije u toku lecenja hipotiroidizma objavili su i drugi autori [20,26]. Garton [12], slicno nasoj studiji, ne uocava signifikantne veze izmedu osteokalcina i bilo kog parametra tiroidne funkcije u toku supstitucione terapije tiroksinom. Nasa studija mora biti interpretirana u okviru njenih ogranicenja. U prvom redu to je kratak pe- riod pracenja bolesnika (prosecno oko 6 meseci) kao i odustvo denzitometrijske evaluacije kostanog sistema. Dugotrajne studije na vecem broju bolesni- ka bi trebalo da odgovore da Ii ubrzanje metabolizma na terapiji l-tiroksinom dovodi do kostanog gubitka i posledicnog rizika od vece ucestalosti fraktura kostiju. Zakljucak Na osnovu izvrsenih ispitivanja mogu se doneti sledeci zakljucci: U nelecenorn hipotiroidizmu kostani metabolizam je usporen u odnosu na eutiroidno stanje. Ovi podaci ukazuju na smanjenu funkciju i osteoblasta i osteoklasta. Uvodenjem supstitucione terapije I-tiroksinom nastaje signifikantan porast metabolickih faktora formiranja kosti i kostane razgradnje u priblizno istoj proporciji. U toku adekvatne supstitucije tiroidnim hormonima, porast nivoa osteoka1cina i crosslaps-e pokazivao je medusobno visoku korelaciju. Ispitivani hormonski i biohemijski parametri metabolizma kalcijuma u toku fizioloske supstitucije tiroidnim hormonima ukazuju na ubrzanje kostanog metabolizma. Nivoi tiroidnih hormona pre terapije pokazuje visoku korelaciju sa parametrima kostanog formiranja i razgradnje, dok se nakon terapije ova korelacija gubi, najverovatnije zbog razlicitog doziranja tiroidnih hormona. Neophodno je duze i kontinuirano pracenje bolesnika na supstitucionoj terapiji I-tiroksinom. Uz kontrolu parametara metabolizma kosti potrebno je periodicno naciniti i morfolosku evaluaciju gustine kosti bolesnika. Odredivanje parametra kostanog metabolizma korisno je u nijansiranoj individualizaciji optimalne supstitucijske doze I-tiroksina. Literatura 1. Mosekilde L, Eriksen EF, Charles P. Effects of thyroid hormone on bone and mineral metabolism. Endocrinol Metab Clin North Am 1990; 19: Allain TJ, McGregor AM. Thyroid hormones and bone..t Endocrinol 1993; 139: Ross OS. Hyperthyroidism, thyroid hormone therapy and bone. Thyroid 1994;4: Langdahl BL, Loft AGR, Eriksen EF, Mosekilde L, Charles P. Bone mass, bone turnover and body composition in former hypothyroid patients receiving replacement therapy. Eur J EndocrinoI1996;134: Cambell J, Day P, Diamond T. Fine adjustments in thyroxine replacement and its effect on bone metabolism. Thyroid 1996;6: Uzzan B, Campos J, Cucherat M, Nony P, Boissel JP, Perret GY Effects on bone mass of long term treatment with thyroid hormones: a meta analysis. J Clin Endocrinol Metab 1996;81 : Hollowe JG, Steahling NW, Flanders WD. Hannon WH, Gunter EW, Spencer CA, et al. Serum TSH. T4 and thyroid antibodies in the United States population ( ): National Health and Nutrition Examination Survey (NHANES Ill). J Clin Endocrinol Metab 2002:87: Canaris GJ, Manowitz NR, Mayor G. Ridgway C. The Colorado thyroid disease prevalence study. Arch Intern Med 2000; 160: Ross OS. Daniels GH, Gouveia D. The use and limitations of a chemiluminescent thyrotropin assey as single thyroid function test in an out-patient endocrine clinic. J Clin Endocrinol Metab 1990;71: Body JJ, Demeester-Mirkine N. Borkowski A Suciu S. Corvilain J. Calcitonin deficiency in primary hypothyroidism. J Clin Endocrinol Metab 1986;62: Garton M. Redl L Loveridge N. Robinst S. Murchison L, Beckett G. et al. Bone mineral density and metabolism in premenopausal women taking L-thyroxine replacement therapy. Clin Endocrinol 1994:41 : Sabuncu T, Aksoy N. Arikan E. Ugur B. Tasan E. Hatemi H. Early changes in parameters of bone and mineral metabolism during therapy for hyper- and hypothyroidism. Endocr Res 2001:27:

5 Med Preg12009; LXII (9-10): Novi Sad: septembar-oktobar Fraser WD. Logue Fe. Mackitchie, Wilson RM. Gray HW. Beastall GH. et a1. Intact parathyroid hormone concentration in cyclic AMP metabolism in thyroid disease. Acta EndocrinoI1991:124: Esedova AE. Gadzhieva MM, Ferzilaeva RA. Calciumphosporus metabolism and bone metabolism in postmenopausal patients with the thyroid gland pathology. Klin Lab Diagn 2002;3: Kisakol G, Kaya A, Gonen S. Tunc Recep. Bone and calcium metabolism in subclinical autoimmune hyperthyroism and hypothyroism. EndocrJ 2003:50: Foscolo G, Roiter L De Menis E, Da Rin G, Legovini P, Conte N. Bone metabolism in primary hypothyroidism in the adult. Minerva Endocrinol 1991;16: Faber.1, Perrild H, Johansen JS. Serum bone Gla protein (BGP) during treatment of hyperthyroidism and hypothyroidism: a longitudinal study. Horm Metab Res 1991 ;23: Nakamura H, Mori T. Genma R. Suzuki Y, Natsume H. Andoh S. et al. Urinary excretion of pyridinoline and deoxyopyridinoline measured by immunoassay in hypothyroidism. Clin Endocrinol 1996;44: Meier C. Muller B. Gugliemetti M, Christ-Crain M. Staub JJ, Kraenzlin M. Restoration of euthyroidism accelerates bone turnover in patients with subclinical hypothyroidism: a randomized controlled trial. Osteoporos Int 2004; 15(3): Summary 20. Stall G. Harris S. Sokoll L. Dawson-Huges B. Accelerated bone loss in hypothyroid patients overtreated with L thyroxine. Ann Intern Med 1990: 113: Knudsen N, Faber J. Sierbaek A. Vadstrup S. Sorensen HA, Hegedus L. Thyroid hormone treatment aiming at reduced. but not suppressed, serum thyroid-stimulating hormone levels in nontoxic goitre: effects on bone metabolism amongst premenopausal women..1 Intern Med 1998;243: Engler H, Oettli RE. Reisen WF. Biochemical markers of bone turnover in patients with thyroid dysfunctions and in euthyroid controls: a cross-selection study. Clin Chim Acta 1999;289: Guo CY. Weetman AP, Eastell R. Longitudinal changes of bone turnover in postmenopausal women on thyroxine. Clin Endocrinol 1997;46: Kojima N, Sakata S, Nakamura S. Nagai K, Takuno H, Ogawa T. et al. Serum concentrations of osteocalcin in patients with hyperthyroidism, hypothyroidism and subacute thyroiditis. J Endocrinol Invest 1992: 15: Gam AN, Jensen GF, Hasselstrom K. Olsen M, Nielsen KS. Effect of thyroxine therapy on bone metabolism in substituted hypothyroid patients with normal or suppressed levels of TSH. J Endocrinol lnvest 199 I:I4: De Rosa G, Testa A, Giacomini D. Carrozza C, Astazi P, Caradonna J. Prospective study of bone loss in pre- and postmenopausal women on L-thyroxine therapy for non-toxic goiter. Clin Endocrinol 1997;47: Introduction The relation between thyroid hormones and bone metabolism markers in hyperthyroidism is well known. Earlier studies indicate the possibility ofbone metabolism acceleration during the excessive replacement therapy with l-thyroxin in hypothyroid patients especially in one with other risk factors for bone metabolism impairment. This study evaluated the effect of physiological l-thyroxine treatment on bone metabolism in patient with primary hypothyroidism. Material and methods In the study group of30 hypothyroidpatients individual thyroxine replacement was performed targeting euthyroid status. Bone and calcium metabolism parameters (osteocalcin-otl, alkaline phosphates-alp, C-terminal cross-linking telopeptide type I-CL, parathormone-pth, Ca, ionized Ca, P), thyroid hormone levels (T3, T4, TSH) were measured before treatment and when euthyroid status was achieved. Results and discussion A significant treatment effect was observed for bone formation and resorption parameters before and during the therapy; OC (p=o ), CL (p=0. (02648). Ionized calcium levels also showed significantly higher values in euthyroid status confirming bone metabolism acceleration during the I-thyroxine therapy (p= 0,(20). Thus, calcium metabolism hormone regulators were not significantly different before and after the therapy; PTH (p=o.27). Thyroid hormone levels showed significant correlation with bone metabolism parameters before the therapy whereas this correlation was not found during therapy because ofdifferent individual I-thyroxine doses. Conclusion It can be concluded that physiological doses ofi-thyroxine therapy accelerate bone metabolism in hypothyroid patients. Thus, the argument against bone loss during physiological substitution is highly specific mutual correlation between bone formation and resorption parameters. These assumptions require further investigations in long term prospective studies in patients on replacement I-thyroxine therapy. Key words: Bone and Bones + metabolism; Hypothyroidism; Thyroxine + therapeutic use; Thyroid Hormones; Bone Resorption Rad je primljen 18. V Prihvacen za stampu 4. XI BIBUD :(2009):LXII:9-1 0:

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