Abstract
NejÄastÄjĹĄĂm typem dÄtskĂŠ obezity, kterĂĄ se vyvĂjĂ v dĹŻsledku kombinace genetickĂ˝ch a environmentĂĄlnĂch faktorĹŻ, je obezita prostĂĄ. PĹĂÄinou sekundĂĄrnĂ obezity mohou bĂ˝t, vedle vzĂĄcnĂ˝ch genetickĂ˝ch forem obezity a vlivu nÄkterĂ˝ch lĂŠkĹŻ, endokrinnĂ choroby, mezi kterĂŠ patĹĂ hypotyreĂłza, CushingĹŻv syndrom, deficit rĹŻstovĂŠho hormonu, hypogonadismus, pseudohypoparatyreĂłza typu Ia, inzulinom, hypotalami ckĂĄ obezita a syndrom polycystickĂ˝ch ovariĂ. ÄasnĂŠ odhalenĂ endokrinnĂ pĹĂÄiny obezity vede ke snĂĹženĂ morbidity a v nÄkterĂ˝ch pĹĂpadech i mortality tÄchto dÄtĂ. Ăkolem lĂŠkaĹe je tyto stavy mezi ostatnĂmi obĂŠznĂmi dÄtmi rozpoznat a ĹeĹĄit. PĹi vyĹĄetĹenĂ pĹĂÄiny obezity je, vedle rodinnĂŠ a osobnĂ anamnĂŠzy, dĹŻleĹžitĂŠ klinickĂŠ a laboratornĂ vyĹĄetĹenĂ, zhodnocenĂ rĹŻstovĂŠ kĹivky a kĹivky BMI (body mass i ndex). Popisujeme patofyziologickĂŠ mechanismy odpovÄdnĂŠ za rozvoj obezity u jednotlivĂ˝ch endokrinopatiĂ, typickĂŠ klinickĂŠ a laboratornĂ nĂĄlezy, patologickĂŠ rĹŻstovĂŠ kĹivky a kĹivky vĂ˝voje BMI vedoucĂ k jejich diagnĂłze.
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