Hashimotova encefaloptia (HE) je ochorenie mozgu združené s autoimúnnym ochorením štítnej žľazy. Doposiaľ bolo publikovaných viac ako 100 prác, najmä v súvislosti s hypotyreózou. Okrem literárneho prehľadu prinášame prípad pacientky so zriedkavou asociáciou HE s tyreotoxikózou. Klinicky sa prezentovala pestrou neurologickou symptomatológiou: mala kŕče, psychotické prejavy, alterované vedomie. Vyšetreniami (laboratórne testy, CT, MRI, EEG, vyšetrenia CSL) zisťujeme zvýšenú hladinu proteínov v likvore, na EEG epizódy rytmickej ? aktivity, zvýšené titre antityreoidálnych protilátok (TPOab, TGAb, TRAb) v sére. Po úvodnej liečbe karbimazolom a hydrokortizónom došlo k výraznému zlepšeniu stavu ? pacientka bola odpojená od umelej pľúcnej ventilácie, bola pri vedomí, bez kŕčov. Počas ďalších 30 dní sa jej stav opakovane zhoršoval po pokusoch o detrakciu glukokortikoidov. Napriek tyreotoxikóze sme stav uzavreli ako HE a po pulznej liečbe metylprednizolonom sa jej stav plne stabilizoval. Klinicky bola pacientka v ďalšom ambulantnom sledovaní bez prejavov encefalopatie, postupne sme detrahovali glukokortikoidy a po 4 mesiacoch bola bez glukokortikoterapie. Záverom autori konštatujú, že HE, aj keď je zriedkavá, môže byť nepoznaná, nakoľko sa prejavuje podobne ako mnohé častejšie ochorenia. Na HE sa má myslieť u pacientov s potenciálnou alebo známou autoimúnnou tyreoitídou s atypickou neuropsychiatrickou manifestáciou odpovedajúcou na liečbu glukokortikoidmi., Juraj Payer, Ľubomír Lisý, L. Baqi, and Lit. 30
Immunomodulatory steroids, dehydroepiandrosterone and its 7-hydroxylated metabolites and sex hormone-binding globulin (SHBG) were determined in sera of 88 women aged 18-75 years. The group consisted of 34 healthy women, 37 women with subclinical and 17 women with manifest hypothyroidism. In all subjects the laboratory parameters of thyroid function (thyrotropin, free thyroxine and triiodothyronine) and thyroid autoantibodies to thyroid peroxidase and thyroglobulin were determined. The aim was to find out 1) whether the above steroids and SHBG levels differ in individual groups according to thyroid status, 2) whether correlations exist among investigated steroids and thyroid laboratory parameters, and 3) whether the respective steroid and SHBG levels differ according to the presence of principal thyroid autoantibodies. With the exception of 7β-hydroxy-dehydroepindrosterone levels, which were decreased in patients with manifest hypothyroidism (p<0.05), no significant differences in steroid and SHBG levels among groups according to diagnosis were found. On the other hand, significantly decreased levels of all the immunomodulatory steroids studied were found in subjects with positive titres of thyroid autoantibodies. This finding was supported by a tight negative correlation among the above steroids and thyroid autoantibodies. In addition, these steroids correlated negatively with thyrotropin and positively with free thyroid hormones. The results point to a negative relationship between the above mentioned immunoprotective steroids and the extent of the autoimmune process in hypothyroidism., K. Drbalová, P. Matucha, M. Matějková-Běhanová, R. Bílek, L. Kříž, H. Kazihnitková, R. Hampl., and Obsahuje bibliografii a bibliografické odkazy
There is accumulating evidence showing that ischemic preconditioning (PC) may lose its cardioprotective effect in the diseased states. The present study investigated whether PC can be effective in hypothyroidism, a clinical condition which is common and often accompanies cardiac diseases such as heart failure and myocardial infarction. Hypothyroidism was induced in rats by 3-week administration of 6n-propyl-2-thiouracil in water (0.05 %). Normal and hypothyroid hearts (HYPO) were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischemia and 45 min of reperfus ion. A preconditioning protocol (PC) was also applied prior to ischemia. HYPO hearts had significantly improved post-ischemic recovery of left ventricular developed pressure, end-diastolic pressure and reduced lactate dehydrogenase release. Furthermore, phospho-JNK and p38 MAPK levels after ischemia and reperfusion were 4.0 and 3.0 fold lower in HYPO as compared to normal hearts ( P<0.05). A different response to PC was observed in normal than in HYPO hearts. PC improved the post-ischemic recovery of function and reduced the extent of injury in normal hearts but had no additional effect on the hypothyroid hearts. This response, in the preconditioned normal hearts, resulted in 2.5 and 1.8 fold smaller expression of the phospho-JNK and phospho-p38 MAPK levels at the end of reperfusion, as compared to non-PC hearts ( P<0.05), while in HYPO hearts, no additional reduction in the phosphorylation of these kinases was observed after PC. Hypothyroid hearts appear to be tolerant to ischemia-reperfusion injury. This response may be, at least in part, due to the down-regulation of ischemia-reperfusion induced activation of JNKs and p38 MAPK kinases. PC is not associated with further reduction in the activation of these kinases in the hypothyroid hearts and fails to confer added protection in those hearts., I. Mourouzis ... [et al.]., and Obsahuje seznam literatury
Onemocnění štítné žlázy tvoří kolem 90 % všech endokrinopatií, postihuje 5–7 % české populace, přičemž ženy jsou postiženy 4–6krát častěji než muži. Z klinického hlediska dělíme tyreopatie na poruchy hormonální produkce a na morfologické postižení. Diagnóza poruchy funkce štítné žlázy vychází ze stanovení hladin tyreoidálních hormonů fT3, fT4 a TSHss v séru. Primární hypotyreóza je charakterizována snížením fT4 a vzestupem TSH. Syndrom nízkého T3 patří k ochranným reakcím organismu, při nichž dochází ke konverzi T4 periferní dejodázou (typu III) na hormonálně neúčinný reverzní trijódtyronin (rT3). U primární hypertyreózy pozorujeme vyšší fT3, fT4 a až neměřitelně nízkou hladinu TSH. Akutní tyreoiditida: známky zánětu a normální tyreoidální funkce, anti-TPO i anti-TG nejsou zvýšeny. Subakutní tyreoiditida probíhá s obrazem zánětu, normálními anti-TPO, anti-TGL, bývá i hypertyreóza. Chronická tyreoiditida, Hashimotova struma patří mezi nejčastější příčiny hypotyreózy u nás a je rozpoznána díky vysokým hodnotám anti-TPO a anti-TG, a vyššímu TSHss. Tyreoidální adenomy a karcinomy jsou klinicky obvykle eutyreoidní. Nezbytné je stanovení nádorových markerů – tyreoglobulinu u papilárního a folikulárního nádoru a kalcitonin u medulárního karcinomu, u kterého je nutné provést genetické vyšetření (stanovení zárodečných bodových mutací, nejčastěji metodou PCR)., Thyroid disorders represent 5–7% of all human diseases, but more than 90% of endocrine diseases and women are affected 4–6-times for often than men. From clinical point of view thyreopathies are distinguished to disorders of hormonal production and to morphological defects. The diagnosis of thyroid function disorder is based on the determination of levels of thyroid hormones fT3, fT4 and TSHss in serum. Primary hypothyreosis is characterized by decreased fT4 and elevated TSH. The syndrome of low T3 belongs to protective reactions of the organism with the conversion of T4 by peripheral deiodinase (Type III) to hormonally ineffective reverse triiodothyronine (rT3). In primary hypothyreosis we observed higher fT3, fT4 and even unmeasurably low level of TSH. Acute thyroiditis: signs of inflammation ad normal thyroidal function, anti-TPO and anti-TG are not elevated. Subacute thyroiditis is characterized with inflammation, normal anti-TPO, anti-TGL, hyperthyreosis may also be present. Chronic thyroiditis, Hashimoto struma belongs to the most frequent causes of hypothyreosis in our conditions and it is usually recognized due to high levels of anti-TPO and anti-TG and higher TSHss. Thyroidal adenomas and carcinomas are usually clinically of euthyroid character. The determination of tumor markers is necessary - thyreoglobulin in papillary and follicular tumor and calcitonin in medullar carcinoma, where a genetic examination (determination of germline point mutations, most often by PCR method) is required., Vlček P., and Lit.: 7