An early stage in T4-induced hyperthyroidism is related to systemic oxidative stress but does not influence the pentose cycle in erythrocytes and systemic inflammatory status

ABSTRACT Objective Hyperthyroidism causes many injuries in its target organs and the consequences are reflected systemically. As systemic alterations in hyperthyroidism at earlier stages have received partial attention, this study aimed to investigate systemic redox and inflammatory status at an early stage of T4-induced hyperthyroidism. Materials and methods Male Wistar rats were assigned to control and hyperthyroid groups (n = 7/group). The hyperthyroid group received L-thyroxine (12 mg/L) in their drinking water for 14 days whereas control group received only the vehicle. Body weight was measured on the 1st and 14th day of the protocol. On the 14th day, animals were anaesthetized. Blood was then collected from the retro-orbital venous plexus and then the animals were euthanised. The blood was separated into plasma and erythrocytes. Plasma was used to measure ROS levels, sulfhydryl compounds, IL-10, TNF-α and LDH levels; erythrocytes were used for the analysis of thioredoxin reductase activity, glutaredoxin content, and pentose cycle enzymes (total G6PD, G6PD and 6PGD). Results Hyperthyroid animals presented body weight gain and final body weight reduction, which was associated with increased ROS levels and decreased sulfhydryl content in plasma. Thioredoxin reductase activity, glutaredoxin content, and pentose cycle enzymes levels in erythrocytes, as well as IL-10, TNF-α and LDH plasma levels were unaltered. Conclusion Taken together, our results suggest an impairment in corporal mass associated with systemic oxidative stress at this stage of hyperthyroidism. Meanwhile, the pentose cycle was not influenced and systemic inflammation and tissue damage seem to be absent at this stage of hyperthyroidism.

Evaluation of redox profiles in exogenous subclinical hyperthyroidism at two different levels of TSH suppression

ABSTRACT Objective: Evaluate the relationship between exogenous subclinical hyperthyroidism and oxidative stress through the analysis of the redox profile of patients with subclinical hyperthyroidism exogenous (SCH) grade I (TSH = 0.1 to 0.4 IU/mL) and grade II (TSH < 0.1 IU/mL). Subjects and methods: We analyzed 46 patients with SCH due to the use of TSH suppressive therapy with LT4 after total thyroidectomy along with 6 control euthyroid individuals (3M and 3W). Patients were divided into two groups, G1 with TSH ≥ 0.1-0.4 IU/mL (n = 25; and 7M 14W) and G2 with TSH < 0.1 IU/mL (n = 25; and 4M 21W). Venous blood samples were collected to measure the levels of markers for oxidative damage (TBARS, FOX and protein carbonylation), muscle and liver damage (CK, AST, ALT, GGT) and antioxidants (GSH, GSSG and catalase). Results: Individuals in G2 showed a GSH/GSSG ratio ~ 30% greater than those in G1 (p = 0.004) and a catalase activity that was 4 times higher (p = 0.005). For lipid peroxidation, the levels measured in G2 were higher than both control and G1 (p = 0.05). No differences were observed for both protein carbonyl markers. G1 and G2 presented with greater indications of cell injury markers than the control group. Conclusion: TSH suppression therapy with LT4 that results in subclinical hyperthyroidism can cause a redox imbalance. The greater antioxidant capacity observed in the more suppressed group was not sufficient to avoid lipid peroxidation and cellular damage.

Neonatal hyper- and hypothyroidism alter the myoglobin gene expression program in adulthood

Myoglobin acts as an oxygen store and a reactive oxygen species acceptor in muscles. We examined myoglobin mRNA in rat cardiac ventricle and skeletal muscles during the first 42 days of life and the impact of transient neonatal hypo- and hyperthyroidism on the myoglobin gene expression pattern. Cardiac ventricle and skeletal muscles of Wistar rats at 7-42 days of life were quickly removed, and myoglobin mRNA was determined by Northern blot analysis. Rats were treated with propylthiouracil (5-10 mg/100 g) and triiodothyronine (0.5-50 µg/100 g) for 5, 15, or 30 days after birth to induce hypo- and hyperthyroidism and euthanized either just after treatment or at 90 days. During postnatal (P) days 7-28, the ventricle myoglobin mRNA remained unchanged, but it gradually increased in skeletal muscle (12-fold). Triiodothyronine treatment, from days P0-P5, increased the skeletal muscle myoglobin mRNA 1.5- to 4.5-fold; a 2.5-fold increase was observed in ventricle muscle, but only when triiodothyronine treatment was extended to day P15. Conversely, hypothyroidism at P5 markedly decreased (60%) ventricular myoglobin mRNA. Moreover, transient hyperthyroidism in the neonatal period increased ventricle myoglobin mRNA (2-fold), and decreased heart rate (5%), fast muscle myoglobin mRNA (30%) and body weight (20%) in adulthood. Transient hypothyroidism in the neonatal period also permanently decreased fast muscle myoglobin mRNA (30%) and body weight (14%). These results indicated that changes in triiodothyronine supply in the neonatal period alter the myoglobin expression program in ventricle and skeletal muscle, leading to specific physiological repercussions and alterations in other parameters in adulthood.

Hipertiroidismo y embarazo / Hyperthyroidism and pregnancy

El hipertiroidismo constituye la enfermedad tiroidea más frecuente de la gestación. Su diagnóstico puede ser algo difícil por los cambios fisiológicos que ocurren durante el embarazo, ambos se acompañan de bocio, hipermetabolismo y circulación hiperdinámica. La dificultad para ganar peso a pesar de mantener el apetito y la taquicardia en reposo (más de 90 latidos/minuto) son los signos más sugestivos. La causa más común (80-85 por ciento) es la enfermedad de Graves, de etiología autoinmune, que aparece con mayor frecuencia en el primer trimestre y el posparto, y puede agravarse si existen niveles elevados de gonadotropina coriónica durante el primer trimestre. El hipertiroidismo manifiesto afecta al curso del embarazo con consecuencias adversas para la madre y el feto. La determinación de niveles elevados de tiroxina y triyodotironina libres es el estudio diagnóstico confirmatorio. El empleo de los antitiroideos de síntesis es la terapia de elección, y se sugiere emplear la dosis mínima necesaria para controlar el hipertiroidismo y mantener a la paciente eutiroidea, lo cual se logra mediante un seguimiento clínico y de la función tiroidea cada 4 o 6 semanas. La lactancia se permite en madres que ingieren dosis de 200 mg/día de propiltiuracilo o 20 mg/día de metimazol(AU)

Hyperthyroidism is the most common thyroid disease in pregnancy. Diagnosing is somewhat difficult because of the physiological changes in pregnancy; it is accompanied with goiter, hypermetabolism and hyperdynamic circulation. Difficulties in gaining weight in spite of keeping appetite and tachycardia value at rest (over 90 beats per minute) are the most suggestive signs. The most common cause (80 to 85 percent of cases) is Graves' disease of autoimmune etiology, which occurs more frequently in the first trimester of pregnancy and after the childbirth, and may become more severe if there are high levels of chorionic gonadotropin during the first trimester of pregnancy. Manifest hyperthyroidism affects the course of pregnancy and has adverse effects for the mother and the fetus. The determination of high levels of free thyroxine and triiodothyronine is the confirmatory diagnostic test. The use of synthesis antithyroid medication is the therapy of choice. The minimal necessary dose is recommended to control hyperthyroidism and to keep the patient in euthyroid state, and this is achieved with clinical and thyroid function follow-up every 4 to 6 weeks. The breast-feeding is allowed in mothers taking a 200 mg/day dose of propylthiouracil or 20mg/day of methimazole(AU)

Influência da função tireoidiana nos níveis séricos de CPK / Influence of thyroid function in CPK serum levels

OBJETIVO: Determinar a variação da CPK sérica em função do TSH e T4 livre (FT4) e avaliar a CPK sérica nos estados patológicos da tireoide (hipertireoidismo e hipotireoidismo), em relação ao eutireoidismo. MATERIAIS E MÉTODOS: Analisaram-se, retrospectivamente, 6.230 exames laboratoriais de 2007 a 2011, com as dosagens de TSH e CPK. Destas, 3.369 com dosagens de FT4. Avaliou-se a correlação entre CPK com TSH e com os estados patológicos da tireoide. RESULTADOS: A correlação entre TSH e CPK foi positiva (r = 0,065), enquanto entre CPK e FT4 foi inversamente proporcional (r = -0,091, p < 0,05). Do total, 586 (9,4%) medidas foram de hipertireoidismo com mediana (intervalo) do CPK de 98 U/L (27 a 1.113) e 556 (8,9%), hipotireóideos com CPK de 114 U/L (25-4.182). CONCLUSÃO: Houve correlação positiva entre CPK sérica e TSH e negativa com FT4, sendo a CPK menor no grupo com hipertireoidismo e maior no grupo de hipotireoidismo.

OBJECTIVE: To determine serum CPK variation based on TSH e free T4 (FT4), and to assess serum CPK in pathological states of the thyroid (hyperthyroidism and hypothyroidism), in relation to the euthyroidism. MATERIAL AND METHODS: We evaluated retrospectively 6,230 laboratory results of TSH and CPK from 2007 to 2011. From these, 3,369 had free T4 results. We evaluated the correlation between CPK and TSH and the pathological states of the thyroid. RESULTS: The correlation between TSH and CPK was positive (r = 0.065), while that between CPK and FT4 was negative (r = -0.091, p < 0.05). From the total of results analyzed, 586 (9.4%) were measures of hyperthyroidism, with a median (range) of CPK of 98 U/L (27 to 1,113), and 556 (8.9%) were of hypothyroidism, with CPK of 114 U/L (25-4,182). CONCLUSION: A positive correlation was found between serum CPK and TSH, and a negative correlation between CPK and FT4. CPK was lower in the group with hyperthyroidism, and greater in that with hypothyroidism.

Imbalance between thyroid hormones and the dopaminergic system might be central to the pathophysiology of restless legs syndrome: a hypothesis

Data collected from medical literature indicate that dopaminergic agonists alleviate Restless Legs Syndrome symptoms while dopaminergic agonists antagonists aggravate them. Dopaminergic agonists is a physiological regulator of thyroid-stimulating hormone. Dopaminergic agonists infusion diminishes the levels of thyroid hormones, which have the ability to provoke restlessness, hyperkinetic states, tremors, and insomnia. Conditions associated with higher levels of thyroid hormones, such as pregnancy or hyperthyroidism, have a higher prevalence of Restless Legs Syndrome symptoms. Low iron levels can cause secondary Restless Legs Syndrome or aggravate symptoms of primary disease as well as diminish enzymatic activities that are involved in dopaminergic agonists production and the degradation of thyroid hormones. Moreover, as a result of low iron levels, dopaminergic agonists diminishes and thyroid hormones increase. Iron therapy improves Restless Legs Syndrome symptoms in iron deprived patients. Medical hypothesis. To discuss the theory that thyroid hormones, when not counterbalanced by dopaminergic agonists, may precipitate the signs and symptoms underpinning Restless Legs Syndrome. The main cause of Restless Legs Syndrome might be an imbalance between the dopaminergic agonists system and thyroid hormones.

Bone and heart abnormalities of subclinical hyperthyroidism in women below the age of 65 years / Anormalidades ósseas e cardíacas do hipertireoidismo subclínico em mulheres com menos de 65 anos

The objective of the present study was to evaluate bone and cardiac abnormalities and symptoms and signs of thyroid hormone excess in women with subclinical hyperthyroidism (SCH) aged < 65 years. Forty-eight women with SCH were evaluated. The control group consisted of 48 euthyroid volunteers. The mean symptom rating scale score was significantly higher in patients. Cardiac involvement, both morphological and affecting systolic and diastolic functions, was also observed in patients. Women with SCH showed a significant increase in serum markers of bone formation and resorption. In addition, bone mineral density (BMD) was lower in the femoral neck but not in the lumbar spine in patients before menopause, whereas a lower BMD was observed at both sites in postmenopausal patients. SCH is not completely asymptomatic in women aged < 65 years, and is associated with heart abnormalities and with increased bone turnover and reduced BMD even before menopause.

O objetivo deste estudo foi avaliar as anormalidades ósseas e cardíacas, sintomas e sinais de excesso de hormônio tireoidiano em mulheres com hipertireoidismo subclínico (HSC) e menos de 65 anos de idade. Quarenta e oito mulheres com HSC foram avaliadas. O grupo-controle consistiu de 48 voluntárias eutireoidianas. A média do escore de sintomas foi significativamente maior em pacientes que em controles. Comprometimento cardíaco, morfológico e afetando as funções sistólica e diastólica, também foi observado. Mulheres com HSC apresentaram significativo aumento dos marcadores séricos de formação e reabsorção óssea. A densidade mineral óssea (DMO) foi menor no colo de fêmur, mas não em coluna lombar em mulheres antes da menopausa; enquanto e em ambos os sítios nas mulheres pós-menopausadas. HSC não é inteiramente assintomático em mulheres com menos de 65 anos, está associado a anormalidades cardíacas morfológicas e funcionais, incremento da remodelação óssea, e menor DMO, mesmo antes da menopausa.

Resposta da paratireóide de ratas às variações do cálcio e fósforo plasmáticos no hipertireoidismo e hipogonadismo / Response of parathyroid to the plasmatic of calcium and phosphorus variations in hyperthyroidism and hypogonadism in the rat

Foram estudadas 84 paratireóides de ratas Wistar com cinco meses de idade, castradas ou não, e mantidas em hipertireoidismo por períodos de 30, 60 e 90 dias. Dois grupos eutireóideos, um castrado e o outro não, foram mantidos nas mesmas condições e serviram de controle. Ao final de cada período, foram colhidos o plasma, para determinação da concentração de T4 livre, o cálcio e o fósforo e as paratireóides, para análise morfológica e determinação da porcentagem de núcleo, citoplasma e estroma. Aos 90 dias houve reversão da hipocalcemia observada aos 60 dias nos animais eutireóideos castrados e não castrados, graças à hipertrofia da paratireóide. O mesmo não ocorreu com os grupos hipertireóideos que apresentaram hipocalcemia e hiperfosfatemia progressivas e não compensadas até os 90 dias. Na castração há pronta reversão da hipocalcemia em resposta ao aumento da atividade funcional da paratireóide. No estado hipertireóideo com gônadas funcionais, apesar da hipertrofia da paratireóide, não há retorno à isocalcemia e isofosfatemia. Na associação hipertireoidismo-castração, a paratireóide não responde satisfatoriamente à hipocalcemia e hiperfosfatemia intensas e progressivas.

La tiroides como modelo de mecanismos moleculares en enfermedades geneticas / The thyroid as a model for molecular mechanisms in genetic diseases

Las enfermedades tiroideas constituyen una heterogénea colección de anormalidades asociadas a mutaciones en los genes responsables en el desarrollo de la tiroides: factor de transcripción tiroideo 1 (TTF-1), factor de transcripción tiroideo 2 (TTF-2) y PAX8, o en uno de los genes que codifican para las proteínas involucradas en la biosíntesis de hormonas tiroideas como tiroglobulina (TG), tiroperoxidasa (TPO),sistema de generación de peróxido de hidrógeno (DUOX2), cotransportdor de Na/I– (NIS), pendrina (PDS), TSH y receptor de TSH. El hipotiroidismo congénito ocurre con una prevalencia de 1 en 4.000 nacidos. Los pacientes coneste síndrome pueden ser divididos en dos grupos: con hipotiroidismo congénito sin bocio (disembriogénesis) o con bocio (dishormonogénesis). El grupo de disembriogénesis, que corresponde al 85% de los casos, resulta de ectopía,agenesia o hipoplasia. En una minoría de estos pacientes, el hipotiroidismo congénito está asociado con mutaciones en los genes TTF-1, TTF-2, PAX-8, TSH o TSHr. La resencia de bocio congénito (15% de los casos) se ha asociado a mutaciones en los genes NIS, TG, TPO, DUOX2 o PDS. El hipotiroidismo congénito por dishormonogénesis es trasmitido en forma autonómica recesiva. Mutaciones somáticas en el TSHr han sido identificadas en adenomas tiroideos hiperfuncionantes. Otra enfermedad tiroidea bien establecida es la resistencia a hormonas tiroideas(RTH). Es un síndrome de reducida respuesta tisular a la acción hormonal causado por mutaciones localizadas en el gen del receptor de hormonas tiroideas (TR). Mutantes de TRinterfieren con la función del receptor normal por un mecanismo de dominancia negativa. En conclusión, la identificación de mutaciones en los genes de expresión tiroidea ha permitido un mayor entendimiento sobre la relación estructura-función de los mismos. La tiroides constituye un excelente modelo para el estudio molecular de las enfermedades genéticas.

Iron Supplementation in Experimental Hyperthyroidism: Effects on Oxidative Stress in Skeletal Muscle Tissue

This study was designed to investigate the effects of iron supplementation on the parameters of oxidative stress in the skeletal muscle tissue of hyperthyroidism induced rats. Hyperthyroidism was found to cause an increase in thiobarbituric acid-reactive substances (TBARS) and copper zinc superoxide dismutase (Cu, Zn SOD) activity, but decreases in the glutathione-peroxidase (GSH Px) activity and glutathione (GSH). Iron supplementation caused an increase in TBARS and a decrease in GSH. Iron supplementation in hyperthyroid rats attenuated the hyperthyroid state, but lowered the plasma ferritin level, which is considered an indicator of thyroid hormone action. Iron supplementation caused no additional increase in the TBARS in hyperthyroid rats, ameliorated the decrease in GSH content and abolished the induction of Cu, Zn SOD. Our findings suggested no increase, but a decrease, in the risk of oxidative stress in iron supplemented hyperthyroid rats. Whether supplementation of iron would have similar effects in humans should be further investigated in clinical studies.

Implantes e suas contra-indicações: protocolo de triagem / Implants and it's contraindications: protocol of screnning

Os autores realizam uma revista da literatura analisando os fatores somáticos sistêmicos que interagem com o sucesso das técnicas de implantodontia oral. Concluem uma conduta protocolar de exames subsidiários, adotada pelo Ceddar - Centro de Estudos e Pesquisas "Prof. Dr. Walter K. Daruge" para a utilização na triagem de pacientes que se submeterão à implantodontia oral com intuito de evitar os efeitos locais da alteração do metabolismo do cálcio geralmente presentes em variadas patologias sistêmicas

Altered metabolism of folates and lipids in hyperthyroid and hypothyroid rats.

Effect of excess folate on the metabolism of folate and plasma lipids in thyroid stressed animals was studied. Administration of excess dietary folate to hyperthyroid rats did not affect the decreased in vivo histidine oxidation in these animals, but it increased the hepatic tetrahydrofolate content. Hypothyroid rats had higher plasma total cholesterol (TC), high density lipoprotein cholesterol (HDLC) and trigylcerides (TG) with no change in post heparin lipolytic activity (PHLA). In hyperthyroidism both TC and HDLC were decreased in plasma and PHLA levels were elevated. On administration of excess dietary folate to hyperthyroid rats HDLC levels were not altered but PHLA and TC levels became near normal, while TG levels remained elevated.

Calorigénesis tiroidea y estres oxidativo celular / Thyroid calorigenesis and cellular oxidative stress

El mantenimiento de la actividad metabólica de la mayoría de los tejidos corporales depende del funcionamiento normal de la glándula tiroidea, la cual sintetiza y libera hormonas (T4, T3) capaces de controlar diversas actividades enzimáticas celulares. El desarrollo de un estado hipertiroideo en vertebrados, además de producir una variedad de síntomas clínicos, aumenta marcadamente la velocidad del metabolismo basal del individuo (Fig. 1), acción conocida como calorigénesis tiroidea, que se caracteriza por un incremento en la velocidad del consumo de O2 total, resultante de los aumentos individuales en la respiración de los tejidos blanco (Fig. 1). Se ha sugerido que la calorigénesis tidoidea está determinada, primeramente, por la interacción de T3 con receptores nucleares de las células blanco, lo cual conduce a un incremento adaptativo en la actividad de enzimas y en el contenido de biomoléculas relacionadas con el metabolismo intermedio y con los sistemas de transporte de electrones celulares. Conjuntamente, se evidencia un aumento en la masa de organelos subcelulares, tales como el retículo endoplásmico liso, mitocondrias y peroxisomas. En la célula hepática se ha demostrado que, como consecuencia de la aceleración del metabolismo oxidativo por la calorigénesis tiroidea, se establece un mayor flujo de electrones a nivel microsomal, mitocondrial y peroxisomal, con un incremento en la generación de O2 -. y/o H2O2 (Fig. 1)

Determinaçäo indireta da testosterona livre através de diálise em equílibrio e sua aplicaçåo em adultos normais e com alteraçöes nos níveis da globulina transportadora dos esteróides sexuais / Indirect determination of free testosterone through equilibrium dialysis, its application in adults with normal and abnormal SHBG levels

A fraçåo livre de testosterona é biologicamente ativa, portnato, importante para avaliaçåo da atividade androogêica. Desenvolvemos uma metodologia para determinaçåo indireta da testosterona livre, baseada em diálise por equilíbrio em soro nåo diluído. Foram dosadas testosterona total e livre, além de SHGB em 54 adultos normais (41 homens e 13 mulheres). Amostras provenientes de 15 pacientes masculinos: 8 acromegálicos e 7 hipertireóideos também foram analisadas e serviram de modelo, respectivamente para as situçöes de diminuiçåo e aumento de SHGB. A reprodutividade do método foi conseguida com a purificaçåo periódica da testosterona triciada, uniformizaçåo do ensaio quanto a duraçåo e temperatura, além da nåo diluiçåo da amostra. Os coeficientes de variaçåo intra e interensaio foram, respectivamente, 0,4 a 22,2 e 4,34 a 43,7 por cento. A técnica, de fácil execuçåo e reprodutibilidade, apresenta sensibilidade para discrimar valores de adultos normais de ambos os sexos, além de evidenciar a distribuiçåo da testosterona em patologias que alteram SHBG

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

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.

Effect of calcium channel blockers on the metabolic changes of hyperthyroidism

To study the effect of calcium channel blocking agents on hyperthyroidism, 14 patients were studied; Wayne's Clinical Diagnostic Index was used for diagnosis and confirmed by estimation of T3 and T4 serum levels. The patients were classified into two groups; group I [seven patients received verapamil alone for one month] and group II [seven patients received a combination of verapamil and carimazole for one month]. After one month's therapy, Wayne's Clinical Diagnostic Index decreased significantly from 35.4 +/- 4.2 [thyrotoxic value] to 10.7 [normal value: up to 10] in group I and from 36.4 4 +/- 2.5 [thyrotoxic value] to euthyroid state [2.29 +/- . 2.20] in group II. The body weight increased in both groups but it was only significant in group II. Also serum T[3] and T[4] levels decreased significantly in both groups. It is concluded that verapamil by itself does not only improve the clinical course of thyrotoxicosis but also decreases the thyroid hormones level centrally and blunts their action peripherally. The combination therapy of verapamil and carbimazole in a smaller dose than used was found to be an efficient and dependable therapeutic line in the medical management of hyperthyroidism. The reduced carbimazole dose which was used successfully in combination with verapamil could be considered as an advantage to avoid the side effects of thiourea drugs

Alteraciones de lípidos y carbohidratos en el bocio tóxico difuso / Lipid and carbohydrate changes in diffuse toxic goiter

Se estudiaron 79 pacientes que padecen de bocio tóxico difuso, de los cuales a 76 se lesrealizó la prueba de la tolerancia a la glucosa, excluyéndose a tres de ellos por tener historia de diabetes mellitus antes del diagnóstico del hipertiroidismo. A la totalidad de los pacientes se les dosificó cifras de colesterol y lípidos totales en sangre. Se constató una frecuencia relativamente alta de tolerancia a la glucosa alterada y diabetes mellitus en nuestra serie. En el estudio de los niveles de colesterol y lípidos totales, se detectaron valores bajos en la mayoría de los pacientes

Influence of thyroid hormone on the phospholipid composition of lung tissue and surfactant of rats.

Thyroid hormone is an important regulator of lipid metabolism in vivo. The effect of thyroid hormone on the phospholipid composition of lung tissue and surfactant has been studied in hypothyroid and hyperthyroid rats in comparison with the control rats. Rats were made hyperthyroid by administering 1 mg of L-thyroxine/kg body weight for six days. Another group of rats was rendered hypothyroid by injecting 1 mci of Na I131 to each rat. Phosphatidyl choline, lysophosphatidyl choline, lysophosphatidyl ethanolamine, phosphatidyl ethanolamine, and sphingomyclin, were estimated by thin layer chromatography. A decrease in phospholipids in hypothyroid and an increase in the hyperthyroid rats was observed. This can be attributed to the altered thyroid activity.