56 resultados para TSH
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OBJETIVOS: comparar os níveis sanguíneos de homocisteína em mulheres com e sem a síndrome dos ovários policísticos (SOP) e correlacioná-los com os parâmetros clínicos, hormonais e metabólicos. MÉTODOS: estudo tipo corte transversal com 110 mulheres: 56 com SOP e 54 controles normais. As pacientes foram submetidas à anamnese, exame físico e ultrassonografia pélvica, dosagens de homocisteína, da proteína C reativa (PCR), glicose, insulina, hormônio folículo-estimulante (FSH), hormônio luteinizante (LH), hormônio tireoide-estimulante (TSH), tiroxina livre (T4L), prolactina e testosterona.. Para análise estatística, foram usados os testes t de Student, χ2 e a correlação de Pearson. A realização da análise multivariada, pelo método "enter", foi utilizada para verificar a associação independente entre as variáveis. RESULTADOS: encontrou-se um aumento significativo na média dos níveis plasmáticos de homocisteína nas pacientes com SOP quando comparadas ao Grupo Controle (5,9±2,9 versus 5,1±1,3 µmol/L; p=0,01). Como era esperado, por fazerem parte do quadro clínico da SOP, o índice de massa corpórea, circunferência abdominal, colesterol total, colesterol HDL, triglicerídeos, insulina e HOMA também se mostraram com diferenças significativas entre os dois grupos. Houve correlação da SOP e do IMC com os níveis de homocisteína. A análise multivariada mostrou que a SOP por si só não se correlaciona com altos níveis de homocisteína. CONCLUSÕES: pacientes com SOP estão expostas a níveis significativamente altos de homocisteína, porém outros fatores intrínsecos à síndrome, e não identificados neste estudo, seriam os responsáveis por esta alteração.
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OBJETIVO: avaliar a associação entre hipotireoidismo e a ocorrência de sintomas depressivos e ansiosos. MÉTODOS: foi realizado um estudo do tipo caso-controle, no período de julho de 2006 a março de 2008, no qual foram incluídas 100 mulheres (50 pacientes com hipotireoidismo primário e 50 controles eutireoidianas) com idade entre 18 e 65 anos. Foram avaliados idade, raça/cor da pele, estado civil, nível educacional, consumo de álcool, situação de trabalho, índice de massa corpórea e estado menopausal. Foram realizadas dosagens de TSH e utilizadas as escalas de ansiedade e de depressão de Beck em todos os casos e controles. O programa utilizado para a análise estatística foi o SPSS, versão 14. O nível de significância adotado foi p<0,05. RESULTADOS: não foram verificadas diferenças significativas entre pacientes com hipotireoidismo primário e controles no que se refere às variáveis demográficas e epidemiológicas. A presença concomitante de ansiedade e depressão foi cinco vezes maior entre os casos do que entre os controles (20 versus 4%; p=0,01). A ocorrência de sintomas ansiosos foi cerca de três vezes maior entre os casos (40%) em relação aos controles (14%) (p=0,003), enquanto a prevalência de sintomas depressivos mostrou-se 75% superior entre casos (28%) quando comparada aos controles (16%) (p=0,15). Neste estudo não foi observada associação entre os níveis de TSH e a prevalência de sintomas de ansiedade e depressão. CONCLUSÕES: este estudo caso-controle apontou uma maior probabilidade de pacientes com hipotireoidismo apresentarem sintomas ansiosos e depressivos em comparação a controles eutireoidianas. Devido às altas prevalências de hipotireoidismo e depressão observadas na prática clínica, a presença de sintomas depressivos deve ser investigada em pacientes com disfunção tireoidiana e pacientes deprimidos devem ser testados com dosagem do TSH.
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OBJETIVO: reavaliar a função adrenal em pacientes com síndrome dos ovários policísticos, após a introdução dos critérios de Roterdã. MÉTODOS: estudo descritivo de corte transversal, incluindo 53 pacientes com média de idade de 26±5,1 anos. Glicose, hemoglobina glicada, lipídios, estradiol, progesterona, 17-OHP4, DHEAS, FSH, LH, TSH, PRL, androstenediona, tiroxina livre, insulina, testosterona total, SHBG e índice de androgênios livres foram estimados. Resistência à insulina, examinada pelo modelo homeostático, foi admitida com índice >2,8. A resposta adrenal à cortrosina foi avaliada pelo incremento hormonal observado após 60 minutos e área sobre a curva. RESULTADOS: entre as 53 pacientes elegíveis, hiperandrogenismo bioquímico foi encontrado em 43 (81,1%). Trinta e três delas, com idade de 25,1±5,0 anos, apresentaram hiperandrogenismo adrenal (62,2%), pesavam 74,9±14,9 kg; tinham IMC de 28,8±6,0 e razão cintura/quadril de 0,8±0,1. DHEAS foi >6,7 nmol/L em 13 (39,4%) e androstenendiona >8,7 nmol/L em 31 (93,9%). Cortisol, 17-OHP4, A e progesterona tiveram incremento de 153%, 163%, 32% e 79%, respectivamente. O modelo usado para avaliar a resistência á insulina foi >2,8 em 14 (42,4%). Não foi encontrada correlação entre as concentrações de insulina ou estradiol com as de cortisol ou androgênios. CONCLUSÕES: a utilização de múltiplos parâmetros hormonais revela alta prevalência de hiperandrogenismo bioquímico na SOP, sendo que as adrenais têm participação em dois terço dos casos. Níveis de estradiol e insulina não influenciam a secreção adrenal de androgênios e cortisol.
Variabilidade da contagem automática tridimensional de folículos ovarianos durante o ciclo menstrual
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Objetivos Avaliar a variabilidade da contagem automática tridimensional dos folículos ovarianos que mediram 2 a 6 mm e 2 a 10 mm durante o ciclo menstrual. Verificar se este exame pode ser aplicado fora da fase folicular precoce do ciclo. Método Prospectivo observacional. Foram incluídas todas as pacientes inférteis submetidas à monitorização da ovulação de 20 de abril de 2013 a 30 de outubro de 2014, com18 a 35 anos; IMC de 18 a 25 kg/m2, eumenorréicas; semhistória de cirurgia ovariana e sem alterações nas dosagens do TSH, prolactina, insulina e glicemia. Foram excluídas aquelas que apresentaram cistos ovarianos e as que faltaram algum dia da monitorização. A contagem ultrassonográfica dos folículos foi feita pelo modo 3D com Sono AVC na fase folicular precoce, folicular media, periovulatória e lútea do ciclo. Resultados Quarenta e cinco mulheres foram incluídas. Houve diferença entre as médias das contagens dos folículos com 2 a 6 mm (p = 0,001) e 2 a 10 mm (p = 0,003) pelo teste de Friedman que avaliou conjuntamente as quatro fases do ciclo. Quando se aplicou o teste t-Student pareado, houve aumento significativo na contagem dos folículos de 2 a 6 mm quando se comparou a contagem desses folículos na fase folicular média e periovulatória com a contagem da fase lútea. Não houve diferença significante entre a contagem destes folículos pequenos nas fases folicular precoce, média e periovulatória. Conclusões A variação da contagem automática tridimensional dos folículos de 2 a 6 mm, nas fases folicular precoce, folicular média e periovulatória, não mostrou significância estatística. Houve uma variação significativa da contagem automática 3D dos folículos ovarianos de 2 a 10 mmdurante o ciclo. A variabilidade significativa da contagem dos folículos de 2 a 10 mm durante o ciclo não permite que este exame seja realizado fora da fase folicular precoce.
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The virulence mechanisms of avian pathogenic Escherichia coli (APEC) have been continually studied and are believed to be multi-factorial. Certain properties are primarily associated with virulent samples and have been identified in avian isolates. In this study a total of 61 E. coli, isolates from chicken flocks with respiratory symptomatology, were probed by Polimerase Chain Reation (PCR) for the presence of genes responsible for the adhesion capacity, P fimbria (papC) e F11 fimbria (felA), colicin production (cvaC), aerobactin presence (iutA), serum resistance (iss), temperature-sensitive hemagglutinin (tsh), and presence of K1 and K5 capsular antigens (kpsII). The iss gene was detected in 73,8%, tsh in 55,7%, iutA in 45,9%, felA in 39,3%, papC in 24,3%, cvaC in 23% and kpsII in18%.
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Escherichia coli isolates from 24 sick psittacine birds were serogrouped and investigated for the presence of genes encoding the following virulence factors: attaching and effacing (eae), enteropathogenic E. coli EAF plasmid (EAF), pili associated with pyelonephritis (pap), S fimbriae (sfa), afimbrial adhesin (afa), capsule K1 (neu), curli (crl, csgA), temperature-sensitive hemagglutinin (tsh), enteroaggregative heat-stable enterotoxin-1 (astA), heat-stable enterotoxin -1 heat labile (LT) and heat stable (STa and STb) enterotoxins, Shiga-like toxins (stx1 and stx2), cytotoxic necrotizing factor 1 (cnf1), haemolysin (hly), aerobactin production (iuc) and serum resistance (iss). The results showed that the isolates belonged to 12 serogroups: O7; O15; O21; O23; O54; O64; O76; O84; O88; O128; O152 and O166. The virulence genes found were: crl in all isolates, pap in 10 isolates, iss in seven isolates, csgA in five isolates, iuc and tsh in three isolates and eae in two isolates. The combination of virulence genes revealed 11 different genotypic patterns. All strains were negative for genes encoding for EAF, EAEC, K1, sfa, afa, hly, cnf, LT, STa, STb, stx1 and stx2. Our findings showed that some E. coli isolated from psittacine birds present the same virulence factors as avian pathogenic E. coli (APEC), uropathogenic E. coli (UPEC) and Enteropathogenic E. coli (EPEC) pathotypes.
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Birds of the Cracidae family (curassows, guans, and chachalacas) are endemic of the Neotropics and 50 species are currently classified. Brazil has 22 species, seven of which are considered threatened. The Alagoas Curassow (Pauxi mitu) species is considered extinct in the wild; but about 120 birds are alive in captivity. Conservation of this species depends entirely on correct management. Health reports of both wildlife and captive curassows are rare. In this study the presence of Escherichia coli was evaluated in 23 healthy Alagoas Curassows from two private breeding centres. E. coli was isolated from cloacal swabs, and the presence of genes encoding cytotoxic necrotising factor 1 (cnf1), alpha-haemolysin (hly), aerobactin (iuc), serum resistance (iss) and the following adhesions: S fimbriae (sfa), pili associated with pyelonephritis (pap) and temperature-sensitive haemagglutinin (tsh) were investigated. E. coli was isolated from 78.3% (18/23) of the birds, and the percentage of curassows colonized by E. coli was similar between the two facilities. From the 22 E. coli isolates, 15 (68.2%) were positive for at least one virulence factor by PCR, and the most frequently found gene was iss (50%). No curassows had clinical signs of disease. Nevertheless, the presence of some E. coli strains may be a concern to the wildlife in captivity. Additional health surveillance studies are essential to guarantee successful conservation programmes for threatened cracids in Brazil.
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This study was designed to evaluate the thyroid and pituitary hormone levels in post-weaning rats whose dams were fed a low-protein diet during suckling (21 days). The dams and pups were divided into 2 groups: a control group fed a diet containing 22% protein that supplies the necessary amount of protein for the rat and is the usual content of protein in most commercial rat chow, and a diet group fed a low-protein (8%) diet in which the protein was substituted by an isocaloric amount of starch. After weaning all dams and pups received the 22% protein diet. Two hours before sacrifice of pups aged 21, 30 and 60 days, a tracer dose (0.6 µCi) of 125I was injected (ip) into each animal. Blood and thyroid glands of pups were collected for the determination of serum T4, T3 and TSH and radioiodine uptake. Low protein diet caused a slight decrease in radioiodine uptake at 21 days, and a significant decrease in T3 levels (128 ± 14 vs 74 ± 9 ng/dl, P<0.05), while T4 levels did not change and TSH was increased slightly. At 30 days, T3 and TSH did not change while there was a significant increase in both T4 levels (4.8 ± 0.3 vs 6.1 ± 0.2 µg/dl, P<0.05) and in radioiodine uptake levels (0.34 ± 0.02 vs 0.50 ± 0.03%/mg thyroid, P<0.05). At 60 days serum T3, T4 and TSH levels were normal, but radioiodine uptake was still significantly increased (0.33 ± 0.02 vs 0.41 ± 0.03%/mg thyroid, P<0.05). Thus, it seems that protein malnutrition of the dams during suckling causes hypothyroidism in the pups at 21 days that has a compensatory mechanism increasing thyroid function after refeeding with a 22% protein diet. The radioiodine uptake still remained altered at 60 days, when all the hormonal serum levels returned to the normal values, suggesting a permanent change in the thyroid function
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Short-term experimental diabetes mellitus (DM) produces a significant decrease in serum thyroid hormones, a decreased or normal serum thyroid-stimulating hormone (TSH) and a reduction in hepatic and renal T4-5'-deiodination. However, little is known about the effects of chronic diabetes mellitus on the pituitary-thyroid axis function. We evaluated the changes induced by very short-term (6 days), short-term (15 days) and chronic (6 months) streptozotocin-induced diabetes mellitus in 3-month old female Dutch-Miranda rat serum T4, serum TSH and T4-5'-deiodinase activity in the thyroid and pituitary glands. Serum hormones were determined by specific radioimmunoassays. Iodothyronine-5'-deiodinase activities were assayed in the thyroid and pituitary microsomal fractions using 2 µM T4 as substrate. Mean serum T4 was significantly decreased from 3.3 to 2.0 µg/dl 6 days after diabetes mellitus induction, and from 2.2 to 1.5 µg/dl after 15 days of DM, with no significant changes in serum TSH, indicating a decreased pituitary TSH responsiveness to the diminished suppression by T4, even though pituitary T4-5'-deiodinase activity was unchanged. Thyroid T4-5'-deiodinase was unchanged after 6 days of diabetes mellitus, but was significantly increased from 20.6 to 37.0 pmol T3/mg protein after 15 days. Six months after diabetes mellitus induction, both serum T4 and thyroid T4-5'-deiodinase returned to normal ranges and serum TSH was unchanged, although pituitary T4-5'-deiodinase was now significantly decreased from 2.7 to 1.7 pmol T3/mg protein. These findings indicate that some kind of adaptation to chronic insulinopenia may occur at the thyroid level, but this does not seem to be true for the pituitary
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Secretion curves for prolactin, cortisol, TSH, and GH from a 37-year old woman with dysthymia and panic disorder with agoraphobia were determined one day prior to (day I), and during a panic attack (day II) associated with an oral dose of 60 mg dl-fenfluramine, a drug known to increase anticipatory anxiety. The increased cortisol secretion observed is discussed in relation to the hormonal correlates of anxiety and the possible role of depression, dl-fenfluramine, and serotonergic receptor sensitivity
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We studied the basal and thyrotropin-releasing hormone (TRH) (50 nM) induced thyrotropin (TSH) release in isolated hemipituitaries of ovariectomized rats treated with near-physiological or high doses of 17-ß-estradiol benzoate (EB; sc, daily for 10 days) or with vehicle (untreated control rats, OVX). One group was sham-operated (normal control). The anterior pituitary glands were incubated in Krebs-Ringer bicarbonate medium, pH 7.4, at 37oC in an atmosphere of 95% O2/5% CO2. Medium and pituitary TSH was measured by specific RIA (NIDDK-RP-3). Ovariectomy induced a decrease (P<0.05) in basal TSH release (normal control = 44.1 ± 7.2; OVX = 14.7 ± 3.0 ng/ml) and tended to reduce TRH-stimulated TSH release (normal control = 33.0 ± 8.1; OVX = 16.6 ± 2.4 ng/ml). The lowest dose of EB (0.7 µg/100 g body weight) did not reverse this alteration, but markedly increased the pituitary TSH content (0.6 ± 0.06 µg/hemipituitary; P<0.05) above that of OVX (0.4 ± 0.03 µg/hemipituitary) and normal rats (0.46 ± 0.03 µg/hemipituitary). The intermediate EB dose (1.4 µg/100 g body weight) induced a nonsignificant tendency to a higher TSH response to TRH compared to OVX and a lower response compared to normal rats. Conversely, in the rats treated with the highest dose (14 µg/100 g body weight), serum 17-ß-estradiol was 17 times higher than normal, and the basal and TRH-stimulated TSH release, as well as the pituitary TSH content, was significantly (P<0.05) reduced compared to normal rats and tended to be even lower than the values observed for the vehicle-treated OVX group, suggesting an inhibitory effect of hyperestrogenism. In conclusion, while reinforcing the concept of a positive physiological regulatory role of estradiol on the TSH response to TRH and on the pituitary stores of the hormone, the present results suggest an inhibitory effect of high levels of estrogen on these responses
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There is little information on the possible effects of estrogen on the activity of 5'-deiodinase (5'-ID), an enzyme responsible for the generation of T3, the biologically active thyroid hormone. In the present study, anterior pituitary sonicates or hepatic and thyroid microsomes from ovariectomized (OVX) rats treated or not with estradiol benzoate (EB, 0.7 or 14 µg/100 g body weight, sc, for 10 days) were assayed for type I 5'-ID (5'-ID-I) and type II 5'-ID (5'-ID-II, only in pituitary) activities. The 5'-ID activity was evaluated by the release of 125I from deiodinated 125I rT3, using specific assay conditions for type I or type II. Serum TSH and free T3 and free T4 were measured by radioimmunoassay. OVX alone induced a reduction in pituitary 5'-ID-I (control = 723.7 ± 67.9 vs OVX = 413.9 ± 26.9; P<0.05), while the EB-treated OVX group showed activity similar to that of the normal group. Thyroid 5'-ID-I showed the same pattern of changes, but these changes were not statistically significant. Pituitary and hepatic 5'-ID-II did not show major alterations. The treatment with the higher EB dose (14 µg), contrary to the results obtained with the lower dose, had no effect on the reduced pituitary 5'-ID-I of OVX rats. However, it induced an important increment of 5'-ID-I in the thyroid gland (0.8 times higher than that of the normal group: control = 131.9 ± 23.7 vs ovx + EB 14 µg = 248.0 ± 31.2; P<0.05), which is associated with increased serum TSH (0.6-fold vs OVX, P<0.05) but normal serum free T3 and free T4. The data suggest that estrogen is a physiological stimulator of anterior pituitary 5'-ID-I and a potent stimulator of the thyroid enzyme when employed at high doses
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Secretion of the a-subunit of pituitary glycoprotein hormones usually follows the secretion of intact gonadotropins and is increased in gonadal failure and decreased in isolated gonadotropin deficiency. The aim of the present study was to determine the levels of the a-subunit in the serum of patients with cirrhosis of the liver and to compare the results obtained for eugonadal cirrhotic patients with those obtained for cirrhotic patients with hypogonadotropic hypogonadism. Forty-seven of 63 patients with cirrhosis (74.6%) presented hypogonadism (which was central in 45 cases and primary in 2), 7 were eugonadal, and 9 women were in normal menopause. The serum a-subunit was measured by the fluorimetric method using monoclonal antibodies. Cross-reactivity with LH, TSH, FSH and hCG was 6.5, 1.2, 4.3 and 1.1%, respectively, with an intra-assay coefficient of variation (CV) of less than 5% and an interassay CV of 5%, and sensitivity limit of 4 ng/l. The serum a-subunit concentration ranged from 36 to 6253 ng/l, with a median of 273 ng/l. The median was 251 ng/l for patients with central hypogonadism and 198 ng/l for eugonadal patients. The correlation between the a-subunit and basal LH levels was significant both in the total sample (r = 0.48, P<0.01) and in the cirrhotic patients with central hypogonadism (r = 0.33, P = 0.02). Among men with central hypogonadism there was a negative correlation between a-subunit levels and total testosterone levels (r = 0.54, P<0.01) as well as free testosterone levels (r = -0.53, P<0.01). In conclusion, although the a-subunit levels are correlated with LH levels, at present they cannot be used as markers for hypogonadism in patients with cirrhosis of the liver.
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The effect of substance P (SP) on thyrotropin (TSH) secretion is controversial. In this study we evaluated the effect of SP on TSH secretion by hemipituitaries of 3-month-old Wistar rats in vitro and its interaction with gastrin-releasing peptide (GRP) at equimolar concentrations (1 µM and 10 µM). TSH release was measured under basal conditions and 30 min after incubation in the absence or presence of SP, GRP or both peptides. Pituitary TSH content was also measured in the pituitary homogenate after incubation. SP at both concentrations caused a significant (P<0.05) increase in TSH secretion compared with all other groups, which was approximately 60% (1 µM) and 85% (10 µM) higher than that of the control group (23.3 ± 3.0 ng/ml). GRP at the lower concentration did not produce a statistically significant change in TSH secretion, whereas at the concentration of 10 µM it produced a 50% reduction in TSH. GRP co-incubated with substance P completely blocked the stimulatory effect of SP at both concentrations. Pituitary TSH content decreased in the SP-treated group compared to controls (0.75 ± 0.03 µg/hemipituitary) at the same proportion as the increase in TSH secretion, and this effect was also blocked when GRP and SP were co-incubated. In conclusion, in an in vitro system, SP increased TSH secretion acting directly at the pituitary level and this effect was blocked by GRP, suggesting that GRP is more potent than SP on TSH secretion, and that this inhibitory effect could be the predominant effect in vivo.
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Although the role of interleukin-2 (IL-2) and interferon gamma (gIFN) is still poorly understood in hyperthyroid diseases, it is reasonable to assume that these cytokines may be present at higher levels in Graves' disease (GD) than in other primarily non-autoimmune thyroid diseases. In order to look for an easy method to distinguish GD from primarily non-autoimmune causes of hyperthyroidism, we compared 13 healthy individuals with 21 treated and untreated hyperthyroid GD patients and with 19 patients with hyperthyroidism due to other etiologies: 7 cases of multinodular goiter, 5 cases of excessive hormone replacement and 7 cases of amiodarone-associated hyperthyroidism. All patients presented low TSH levels and a dubious clinical thyroid state. We found a good correlation between TSH and serum IL-2 levels (r = 0.56; P<0.01). Serum IL-2 (P<0.01) and gIFN (P<0.01) levels were lower in the hyperthyroid group of patients than in control subjects, suggesting a depressed TH1 pattern in the T-cell subset of hyperthyroid patients. GD had normal IL-2 levels, while patients with other forms of thyrotoxicosis presented decreased IL-2 levels (P<0.05). There was no difference between treated and untreated GD patients. We suggest that the direct measurement of serum IL-2 level may help to confirm hyperthyroidism caused by GD.