Q12 cáncer diferenciado de tiroides (CDT): estimulación de la TSH endógena con múltiples dosis de TRH y su tratamiento con 131I: experiencia de 3 años / Differentiated thyroid carcinoma: endogenous TSH stimulation by multiple dosage of TRH and treatment with 131I

La búsqueda un método alternativo a la rh-TSH para estimular el aumento de la TSH sérica previo al tratamiento con 131I en pacientes con CDT operados con reducción del tiempo del hipotiroidismo pre ablativo fue el propósito del trabajo que iniciamos en el año 2001 en el Paraguay utilizando múltiples dosis de TRH para estimular la TSH endógena de los pacientes para luego lograr la ablación del remanente tiroideo con 131I. Se conoce que la inyección de una dosis única de 200µU de TRH por vía EV logra el aumento de la TSH endógena en los pacientes con carcinoma diferenciado de tiroides logrando elevar la TSH entre 30 - 35 mUI/L al final de la primera hora , sin embargo, no se cuentan con datos estadísticos de los efectos de múltiples inyecciones de TRH aplicadas por vía EV o por vía IM en los pacientes operados de tiroides por CDT previamente a la ablación con 131I. Material y Método: Desde el 2001al 2007 doscientos pacientes operados por CDT fueron estudiados por este método en el Centro de Diagnostico y Tratamiento Nuclear (CEDIN), 120 correspondieron a cáncer papilar y 80 a cáncer folicular. Ciento ochenta no presentaron metástasis a distancia y 20 presentaron metástasis en cuello, tórax, pelvis y columna dorsal. Tiroidectomía total se realizó en 120 y lobectomía total e itsmectomía más hemilobectomía del lado contra lateral en 80. Todos fueron tratados con dosis ablativas (100 mCi (3.700 mBq) de 131I excepto aquellos con metástasis que recibieron 150 mCi (5.500 mBq) previa estimulación con TRH por vía EV en dos dosis diarias por dos días con previa suspensión de L-tiroxina por 25 días antes del tratamiento reemplazándola por triyodotironina 25 mcg/día por 15 días tras lo cual también fue suspendida 10 días antes de la estimulación con TRH y el tratamiento con 131I. Dos pacientes con metástasis recibieron otra dosis extra de 150 mCi (5.550 MBq) 6 meses después...

The search of an alternative method to the rh-TSH to stimulate endogenous rising of TSH previous to thyroid ablation with 131I in patients with CDT operated. The purpose of the work began in 2001 in Paraguay using multiple dose of TRH IV (200µU of TRH Threlea® Argentina) to stimulate the own TSH of patients previous to 131I ablation. It is known that the injection of an unique dose of 200µU of TRH IV achieves the increasing of the endogenous TSH in patients with differentiated thyroid carcinoma up to 30 - 35 mUI/L at the end of the first hour, however, there is not statistical data of the effects of multiple injections of TRH applied IV or IM in operated patients of DTC previous to the ablation with 131I. Since 2001-2007, two hundred patients operated for DTC were studied by this method, 120 were papillary cancer and 80 follicular cancer. One hundred eighty did not have distance metastasis and 20 presented metastasis in thorax, pelvis and dorsal spine. Total thyroidectomy was carried out in 120 and total lobectomy with itsmectomy plus hemilobectomy of the other lobe in 80. All were treated with ablative dose of 100 mCi (3.700 mBq) of 131I, except those with metastasis which receive 150 mCi (5.500 mBq) with the previous stimulation with TRH IV with two daily dose for three days with previous suspension of L-tiroxine for 25 days and replaced by triyodotiroxine 25 mcg/d for 15 days with suspension 10 days before the stimulation with TRH and treatment with 131I. Two patients with metastasis received another extra dose of 150 mCi (5.550 MBq) 6 months later. One presented uptake in thyroid bed one year after the ablation received a new ablative dose of 100 mCi (3.700 mBq) of 131I. All the patients were interned and isolated by 48 hours. Twenty feminine patients had later pregnancies in 1-3 years after their ablative dose with healthy products. TSH was measured during the stimulation with TRH in all patients...

Función tiroidea en pacientes pediátricos con enfermedad renal crónica / Thyroid function in pediatric patients with chronic renal failure

Objective: To characterize the thyroid function in mild (L), moderate (M), hemodialysis (HD), peritoneal dialysis (PD), chronic renal failure (CRE) and post kidney transplant (TX). Method: 46 children between 9.3 +/- 3.7 years-old with CRF (10 mild (L), 10 moderate (M), 10 peritoneodialysis (PD), 6 hemodialysis (HD), 10 transplants (TX)) were evaluated. Basal total T4 and free T3, TRH test (TSH at 0-30-60 min), creatinine, BUN, creatinine clearance and anthropometric parameters were measured. The statistics analysis included Anova Test to compare group results and correlation coefficients for studied variables. Results: Basal thyroid hormone levéis were normal in all groups and no differences between groups (except higher TSH in L (p < 0.01)) were found. TRH test response was prolonged on L, M, PD and HD and deficient in TX, except 3 TX patients who had normal TRH response, all using Tacrolimus, Micofenolate and Prednisone on altérnate day treatment versus the remaining TX who where on Cyclosporine or Azathioprine, Micofenolate and continuous corticoid régimen. Prolonged TRH response correlates with creatinine (p < 0.001) and creatinine clearance (p < 0,01). Conclusions: Basal thyroid hormones were normal in all groups. TRH test response was predominantly prolonged in L, M, PD and HD, suggesting adaptative phenomena at tertiary level, and correlates with renal function. TX patients had deficient TRH response, suggesting hypofisial dysfunction.

Objetivo: Caracterizar la función tiroidea y la respuesta a test de TRH (thyroid releasing hormone), en niños con enfermedad renal crónica (ERC) leve (L), moderada (M), peritoneodiálisis (PD), hemodiálisis (HD) y trasplantados renales (TX). Pacientes y Método: Se estudiaron 46 pacientes con ERC (10 L, 10 M, 10PD,6HDy 10TX),9,3 +/- 3,7 años. Se midió t4t,t41,t3t, t31,TBGbasalytest de TRH(TSHa 0,30y60min). Se evaluó función renal, antropometría y se consignó tratamiento inmunosupresor (IS) en el grupo TX. Se utilizó anova para comparar los resultados entre los grupos y coeficiente de correlación para las variables estudiadas. Resultados: Los valores basales de hormonas tiroideas fueron normales en todos los grupos, sólo TSH fue significativamente mayor en L aunque dentro del rango normal (p < 0,01). La respuesta al test de TRH fue predominantemente prolongada en L, M, PD y HD y deficiente en TX; los 3 pacientes TX con tacrolimus, micofenolato y prednisona en días alternos tuvieron respuesta normal a diferencia del resto TX que recibían prednisona continua, ciclosporina y micofenolato. La prolongación de respuesta a TRH se correlacionó con creatininemia, BUN y clearance de creatinina (p < 0,01). Conclusiones: Los niveles de hormonas tiroideas basales se encuentran normales en todos los grupos de ERC. La respuesta a TRH fue predominantemente prolongada en L, M, PD y HD, demostrando un fenómeno adaptativo a nivel terciario del eje hipotálamo-hipofisis-tiroides. Los TX presentan una respuesta mayoritoriamente deficiente a TRH, sugerente de disfunción hipofisiaria, la que podría estar relacionada con el tipo de tratamiento inmunosupresor y al uso de corticoides en días continuos.

Efecto de la hormona liberadora de tirotrofina en la secreción de prolactina de decidua humana / Effect of thyrotropin releasing hormone in the prolactin secretion of human decidua

Para prevenir el síndrome de distress respiratorio (RDS), se ha usado el tratamiento conjunto de betametasona y hormona liberadora de tirotrofina (TRH). La TRH actuaría indirectamente sobre la producción del surfactante pulmonar, estimulando la secreción de hormonas tiroídeas; otra vía para incrementar el surfactante pulmonar es induciendo la secreción de PRL Prolactina (un potente estimulador de la secreción del surfactante pulmonar) desde la hipófisis o de otros tejidos que secreten PRL (como se ha descrito previamente para la decidua). El objetivo de este trabajo fue estudiar el efecto de diferentes dosis de TRH en la secreción de PRL por el tejido corión-decidua y caracterizar las formas bioactivas de PRL secretada por dicho tejido. Veinte placentas de embarazos normales (38-41 semenas), obtenidas por parto normal o cesáreas, fueron recolectadas en el Departamento de Obstetricia y Ginecología del Hospital Clínico de la Universidad de chile. Explantes de tejido corión-decidua secretaron PRL en condiciones basales, con una secreción máxima de la hormona a las 24 horas de incubación. Se encontró un aumento significativo (p<0,05) en la secreción de PRL con 1,5 x 10 elevado 8 M de TRH, el cual fue debido principalmente a un aumento significativo (p<0,05) de la forma little del PRL bioactivo. Estos resultados sugieren que una de las maneras en que TRH acelere la madurez pulmonar fetal podría ser aumentando la secreción de PRL por el tejido decidual; esta hormona podría pasar rápidamente al líquido amniótico para activar la producción del surfactante pulmonar del feto

Thyrotropin releasing hormone injected into the nucleus accumbens septi selectively increases face grooming in rats

The effect of unilateral injection of peptides into the nucleus accumbens septi (NAS) on subcategories of grooming behavior was studied in male rats. The peptides used were: thyrotropin releasing hormone (TRH), luteinizing hormone releasing hormone (LHRH) and corticotropin releasing hormone (CRH). Male rats (Holtzman strain, 240-270 g body weight) injected with progressive doses of TRH (100, 200 and 400 ng) at 5-day intervals were compared with the control state (injection of artificial cerebrospinal fluid CSF). A selective increase in face grooming was observed with the 100 ng (49.78 + 6.11, N = 18) and 200 ng (50.29 + 7.72, N = 17) doses of TRH (P<0.05 vs CSF injection 26.94 + 3.64, N = 18). Face grooming increased further with the 400 ng dose (55.19 + 8.26, N = 16, P<0.01), but a dose-response curve could not be obtained at the dose range used. Flank scratching, head, body and genital grooming were not altered by the TRH injection, but the rearing behavior was inhibited (10.33 + 1.56; N = 18; 10.76 + 1.77, N = 17; 12 + 2.06, N = 16) (P<0.05 for all doses vs controls, 20.61 + 2.81, N = 18). The rats that received LHRH (75 ng, N = 16) and CRH (100 ng, N = 14) did not show behavioral changes when compared with their control states. The results show that injection on TRH into the NAS, but not the injection of LHRH or CRH, selectively increases face grooming without affecting other subcategories of grooming at the doses used, and appears to link this peptide with the neural substrate of stereotyped behavior.

Distinct grooming patterns induced by intracerebroventricular injection of CRH, TRH and LHRH in male rats

This paper reports the effects on grooming, related behaviors and levels of anxiety induced by the hypophysiotropic peptides corticotropin-releasing hormone (CRH, 1 mug, 0.2 nmol, icv), thyrotropin-releasing hormone (TRH, 100 mug, 275 nmol, icv) and luteinizing hormone-releasing hormone (LHRH, 1.5 mug, 1.3 nmol, icv) administered into the lateral ventricle of the brain (icv) of adult male rats of a Holtzman-derived colony (N = 15, each group). CRH induced an increase in total grooming scores, whereas LHRH, TRH and vehicle had no effect. CRH strongly increased face and head grooming and induced head shakes. The time spent in rearing and gnawing was significantly decreased. In the plus-maze, CRH reduced the time of exploration in the open arm. TRH increased face grooming and induced body shakes. LHRH had no effect on grooming or rearing behavior. No body or head shakes were observed after LHRH administration. Scoring of individual grooming elements demonstrated differences in action of the three peptides. Although both CRH and TRH increased face grooming, only CRH induced head grooming. Furthermore, CRH induced predominantly head shakes while TRH increased body shake activity. In contrast, CRH was anxiogenic and TRH appeared to induce stereotyped behavior. From the characterization of grooming elements and related responses, we conclude that each hypophysiotropic peptide induces a specific behavioral pattern.

Paradoxical effect of neuromedin B and thyroxin on thyrotropin secretion from isolated hyperthyroid pituitaries

Neuromedin B (NB) is a bombesin-like peptide that we recently characterized as a physiological autocrine inhibitor of thyrotropin (TSH) secretion. We now report the effect of NB, thyroxin (T4) and NB + thyroxin on basal and THR (50 nM)-stimulated TSH release from isolated hemipituitaries of hyperthyroid rats. To induce hyperthyroidism, 20 rats were treated with 0.03 per cent methimazole for one month and then received T4, 4 micrograms/100 g body weight, sc, daily for 7 days. Each experimental group consisted of 7 to 9 hemipituitaries. TSH was measured using a rat TSH kit provided by NIDDK. Basal TSH release was paradoxically increased in the presence of 0.1 microM T4 or 0.1 microM NB and even two times higher in the presence of both (Control: 30.0 +/- 4.2 ng/ml; T4: 58.6 +/- 5.6 ng/ml; NB: 53.4 +/- 6.1 ng/ml; T4 + NB: 90.4 +/- 8.5 ng/ml). The percent increment above basal TSH levels after TRH was higher only in the presence of NB (Control: 44.5 +/- 8.2 per cent , NB: 105.3 +/- 18.8 per cent ; P < 0.05). Altered responsiveness in hyperthyroidism and direct modification of the intracellular metabolism of T4 are mechanisms that could explain this paradoxical effect

Thyrotropin releasing hormone-induced potentiation of spinal monosynaptic reflex in rats in vitro.

Superfusion of thyrotropin-releasing hormone (TRH) in neonatal rat spinal cord in vitro produced dose (0.01-1.00 microM) dependent potentiation of monosynaptic reflex (MSR) which was maximum (44% of control) at 1 microM of TRH. But no ventral root depolarization was observed with TRH (1 microM) although potassium concentration out side ([K+]0) when increased produced a depolarization at the magnitude of 0.2 mV/mM of [K+]0. TRH-induced potentiation of MSR was not altered in spinal cords, obtained from the animals pretreated with 5,7-dihydroxytryptamine or 6-hydroxydopamine. Neither serotonin antagonists (spiperone, ketanserin, cyproheptadine or 3-troponyl-indole-3-carboxylate) nor adrenergic antagonists (phentolamine or haloperidol) could attenuate TRH-induced potentiation. Inhibition of MSR observed in the spinal cord elicited by stimulating the adjacent dorsal root was unaffected by TRH. The results suggest that, TRH potentiates MSR by directly acting on the motoneurons, without involving presynaptic serotonergic or catecholaminergic neuronal systems or the disinhibition of pre- or post-synaptic inhibition in the spinal cord.

Hormonal modulation of biosynthesis of prostatic specific antigen, prostate specific acid phosphatase and prostatic inhibin peptide.

Hormonal modulation of in vitro biosynthesis of three prostatic secretory proteins, prostate specific acid phosphatase (PSAP), prostate specific antigen (PSA) and prostatic inhibin peptide (PIP) by human benign hyperplasia (BPH) tissue was studied. LH and inhibins caused increase in the synthesis of all three proteins whereas FSH enhanced the synthesis of PIP and PSA only but decreased PSAP synthesis. Prolactin and thyroid releasing hormone decreased synthesis of PIP and PSAP. However, PSA synthesis was enhanced by TRH and was decreased by prolactin. Estradiol caused significant increase in PSA and PSAP but no discernible changes in PIP synthesis were noticed. Testosterone caused an increase in PIP, PSA and PSAP. These data indicate that biosynthesis of PIP, PSA and PSAP by BPH tissue is under multihormonal regulation.

Synergistic effect of cortisol and thyrotrophin releasing hormone on lung maturation in the fetal sheep entails connective tissue maturation

Pressure-volume relationships and collagen and elastin contents were measured in the lungs of fetal sheep infused either with saline (n = 4), thyrotrophin-releasing hormone (TRH; n = 6), cortisol (n = 9) or TRH plus cortisol (n = 10) at 128 days of gestation (term = 149 days) for 7 days. Lung distensibility (V40 = 1.8 +/- 0.1 ml/g wet wt; mean +/- SD) and stability (V5 = 0.6 +/- 0.1) increased along with collagen (C) (10.1 +/- 2.7 micrograms/mg) and elastin (E) contents (128 +/- 35 ng/mg) in the animals infused with TRH plus cortisol and were significantly higher (p < 0.05) than those observed in TRH (V40 0.62 +/- 0.07; V5 0.32 +/- 0.04; C 3.53 +/- 1.3; E 38.2 +/- 8.3), cortisol (V4 0.66 +/- 0.6; V5 0.27 +/- 0.03; C 4.27 +/- 0.8; E 41.02 +/- 12.7) or saline infused fetuses (V40 0.40 +/- 0.1; V5 0.20 +/- 0.06; C 3.28 +/- 0.9; E 31.5 +/- 9.2). Plasma concentrations of prolactin (PRL), triiodothyronine (T3) and cortisol (F) were also higher in the group of fetuses infused with both hormones in comparison with the other groups. In fetuses treated with TRH plus cortisol, PRL (32 +/- 8.3 ng/ml) and T3 (308.3 +/- 36 micrograms/dl) were significantly higher than in those infused with cortisol alone (PRL 3.7 +/- 2.3; T3 128 +/- 30) or with saline (PRL 4.2 +/- 1.6; T3 < 5 micrograms/dl). In the group treated with TRH alone, PRL also increased significantly (37 +/- 6.4), but T3 increased only slightly (18 +/- 3.4).(ABSTRACT TRUNCATED AT 250 WORDS)

Avaliaçäo da resposta do T3 livre, TT3 e TSH ao teste do TRH em indivíduos normais, hipotireóideos e hipertireóideos / Evaluation of the free T3, TT3 and TSH response to the TRH test in normal, hypothyroid and hyperthyroid subjects

O ensaio do T3 livre näo é influenciado pelas proteínas séricas circulantes, e sendo este o hormônio ativo, nos propusemos a estudar o T3 livre no teste do TRH em 15 indivíduos (seis normais, quatro hipertireóideos e cinco hipotireóideos), que foram submetidos à infusäo aguda de TRH (200µg EV) quantificando-se no soro, além da fraçäo livre do T3, o T3 total e o TSH. A maior variaçäo percentual de triiodotironina total nos normais ocorreu aos 180 minutos após o TRH (23,9 por cento), näo estatísticamente significativa. A maior variaçäo de FT3 ocorreu aos noventa minutos , com aumento de 88, 9 por cento (p<0,005). Os incrementos percentuais relativos (delta por cento = pico basal/basal) x 100 do T3 livre foram significativamente maiores nos indivíduos normais que nos hipertireóideos (p<0,05) e ainda significativamente menores nos hiperteireóideos (p<0,05). Em conclusäo, a utilizaçäo da determinaçäo do T3 livre nos testes de infusäo aguda de TRH nos permite a concomitante avaliaçäo da reserva pituitária de TSH e da capacidade de secreçäo tireoideana de triiodotironina na sua forma livre, podendo ser útil no diagnóstico diferencial dos distúrbios tireoideanos.

Endogenous hyperinsulinemia and release of growth hormone following a glucose load as well as in reponse to thyrotropin relasisng hormone in acromegaly

This study was designed to determine the relationship between endogenous hyperinsulinemia or free fatty acid (FFA) levels and the abnormal release of growth hormone (GH) during the oral glucose tolerance test (OGTT) or in response to thyrotropin releasing hormone (TRH) in acromegalic patients. Seventeen patients with acromegaly and nine healthy control subjects were studied. The 12 acromegalic patients who did not show the paradoxical response of increased GH secretion to the OGTT an/or to TRH exhibited higher insulin levels (total area under the curve during the OGTT) than patients who did. However, the FFA levels of the groups of acromegalic patients were similar. These data suggest that the endogenous hyperinsulinemia exhibited by many patients with acromegaly is associated with the absence of the paradoxical increase in GH secretion during the OGTT and/or after TRH

Effects of prostatic inhibin and thyroid releasing hormone on lipid peroxidation in rat prostate.

Effects of prostatic inhibin and thyroid releasing hormone (TRH) on lipid peroxidation in rat prostate was studied in an in vitro system. It was found that both inhibited the lipid peroxidase activity thus having a protective role in the prostate.

Immediate effects of intermitent administration of domperidone upon prolactin release in normal women

El presente, estudio fue llevado a cabo con la finalidad de investigar el efecto de la administración repetida del antagonista dopaminérgico domperidone (DOM) sobre la secreción de prolactina, así como la respuestas de esta hormona a la administración de la hormona liberadora de tirotrofina (TRH) durante el efecto máximo del antagonista. Se estudiaron 9 mujeres normales durante la fase folicular del ciclo menstrual, las cuales fueron divididas en 3 grupos de acuerdo al siguiente diseño: I. Administración repetida de DOM (10 mg cada 60 minutos por 3 horas), seguida de un bolo i.v. de TRH (200 ug). II. Bolos intermitentes de DOM (10 mg cada 60 minutos por 2 horas), seguidos de TRH, 200 ug. i.v. al tiempo de la tercera inyección del DOM, y III. Bolos intermitentes de DOM (10 mg/hora por 3 horas), seguidas de 10 mg i.v. de metoclopramida al momento de la última dosis de DOM, así como de 200 g de TRH administrados 90 minutos después del bolo de DOM + metoclopramida. Las concentraciones plasmáticas de PRL inmunorreactiva fueron cuantificados antes y a intervalos de 15 a 30 minutos durante los experimentos. Treinta minutos después del primer bolo de DOM, todos los sujetos mostraron un incremento significativo en las concentraciones séricas de prolactina (PRL); posteriormente, dichas concentraciones disminuyeron progresivamente a pesar de bolos adicionales del antagonista. Igualmente, la administración de metoclopramida al tiempo de la refractariedad hipofisiaria al DOM, fue incapaz de incrementar las concentraciones séricas de PRL. Todos los sujetos respondieron a TRH sin importar el momento de la inyección, las concentraciones séricas de PRL presentes o las manipulaciones farmacológicas precedentes (administración de DOM y/o metoclopramida). La cinética de liberación de PRL durante estas manipulaciones farmacológicas pudieran ser explicadas por el efecto agonista-antagonista del DOM sobre la secreción del lactotropo. Más aún, la presencia de una respuesta a significativa a TRH durante períodos de refractariedad al DOM, sugiere la existencia de 2 pozas de PRL en el lactotropo humano, una de ellas regulada por dopamina en tanto que la segunda por un factor liberador de PRL y/o por TRH

Teste do TRH: padronizaçäo das respostas do TSH e prolactina em homens e mulheres em diferentes faixas etárias / TRH test: standardization of TSH and prolactin responses in men and women at different age groups

A medida do TSH e PRL após injeçäo de TRH constitui um teste funcional endócrino amplamente utilizado. Diferentes graus de resposta do TSH e PRL podem ocorrer em funçäo do sexo e da faixa etária, tornando-se, portanto, importante estabelecer um padräo de resposta normal que leve em consideraçäo estas variáveis. Com este objetivo, os níveis plasmáticos do TSH e PRL aos 20 e 60 minutos após a administraçäo endovenosa de 200 µg de THR (Laboratório de Biofísica da escola paulista de Medicina)foram medidos em 23 individuos normais, divididos em 4 grupos , de acordo com o sexo (homens e mulheres) a faixa etária (20 a 40 anos e 40 a 60 anos). Quanto à resposta do TSH ao TRH, observou-se que a resposta máxima ocorreu aos 20 minutos, näo sendo necessária medida aos 60 minutos; näo houve modificaçäo de resposta com a idade em homens e mulheres; mulheres de de 20 a 40 anos responderam mais do que homens de 20 a 40 anos (20 minutos) e mais do que o homem de 40 a 60 anos (20 a 60 minutos); o aumento mínimo considerado normal para os homens foi de 2,6 µ UI/ml e, para as mulheres , de 4,5 µ UI/ml. Em relaçäo à resposta da PRL ao TRH, constatou-se que a resposta máxima ocorreu aos 20 minutos, näo sendo necessária medida aos 60 minutos; näo houve diminuiçäo de resposta com a idade em mulheres (20 a 60 minutos) e em homens (20 minutos); as mulheres responderam mais do que os homens nas faixas etárias estudadas, o aumento mínimo considerado normal para os homens foi de 6ng/ml ou 0,5 vez o valor basal e, para as mulheres, de 50ng/ml ou 3 vezes o valor basal.

Funçäo tireoidian e produçäo de AMP cíclico em nódulos autônomos da tiróide / Thyroid function and cyclic AMP production in autonomous thyroid nodules

Foram estudadas cinco pacientes eutiroidianas portadores de nódulos autônomos à cintilografia tireiodiana, com diàmetro superio a 3cm e näo supressíveis pela administraçäo de T, (100µg/dia durante 10 dias). Quatro das pacientes apresentaram exames laboratoriais (T4 livre, T3 TSH basal e captaçäo de 131I em 24h) normais. Fatias de tecido tireoidiano adenomatoso e paranodular obtidas pela tiroidectomia foram incubadas com concentraçöes crescentes de TSH e na presença ou näo de iodeto de potássio (KI)ou triiodotironina (T3). O incremento da produçäo de AMP cíclico (cAMP) provocado pelo TSH no tecido adenomatoso foi igual ao encontrado do tecido adjacente paranodular. No tecido paranodular a adiçäo de T3 ou KI inibiu significativamente a produçäo de cAMP, enquanto que, no tecido adenomatoso, a açäo inibitória ocorreu apenas com KI. Estes resultados sugerem: 1) a inibiçäo da secreçäo pode ocorrer na presença de níveis hormonais tiroidianos circulantes normais; 2) nâo há evidência de sensibilidade aumentada ao TSH no tecido autônomo quando avaliada pela produçäo de cAMP; 3) a ausência inibitória do T, na resposta do TSH no tecido nodular sugere alteraçäo celular ao nível de outros reguladores da geraçäo de cAMP.