Le dosage de la thyroxine et de la tri-iodothyronine libres sériques doit-il supplanter les autres méthodes d'évaluation de la fonction thyroïdienne ?

Total T4, total T3, free T4 and free T3 were measured at the same time in 633 subjects. These subjects were classified according to the clinic state and the hormonal results in 426 euthyroid, 145 hyperthyroid and 62 hypothyroid cases. The results permitted to define the sensitivity, specificity and predictive value of the different tests. When each measure was considered alone, free T4 was the most useful test for all the hormonal states. In association, FT4 + FT3 is more useful than T3T + T4T for all the diagnostic parameters and for all the clinical situations. To measure FT4 with an adequate kit appears to be in 1985 the key method for evaluating the thyro?d function. To associate FT3 is useful in some difficult cases.     

Studies on the effect of thyroxine onin vivo insulin secretion as modified by hypophysectomy

Summary Blood sugar and serum immunoreactive insulin (IRI) concentrations were measured in uninjected and thyroxine-injected hypophysectomized dogs as well as in untreated normal dogs. Thyroxine was used at the following two levels: 0.5 and 100 /kg body wt./day, for 10 days. Serum IRI levels in the dog in the post-absorptive conditions were unaffected by both treatments. Mildly subnormal blood sugar levels were detected, in the hypophysectomized dog in the post-absorptive condition and were fully corrected by thyroxine therapy (both levels). The rate of disappearance of glucose from the blood was normal in the hypophysectomized control dogs and was unaffected by thyroxine therapy. The moderate increase in the general mean of the blood sugar throughout the test found after hypophysectomy was corrected by thyroxine (low level); thyroxine therapy (high dose) not only failed to correct the increase but in fact induced a further increase. The typical slow, low and maintained insulin response to hyperglycaemia was found in the hypophysectomized control dogs, and it remained unchanged despite the thyroxine treatment (both levels). We concluded that the presence of the pituitary gland is needed so that the thyroxine-induced inhibition of the insulin secretory response to hyperglycaemiain vivo may be exerted.This paper was partially presented at the Meetings of the VII Congress Intern. Diabetes Fedn, Buenos Aires, Argentina, 23–8 August, 1970.     

Thyroid response to dexamethasone: A study on normal controls and patients with psychogenic sexual dysfunction: Der Einfluß von Dexamethason auf die Schilddrüsenfunktion bei Patienten mit erektiler Dysfunktion und gesunden Männern

Pre- and postdexamethasone triiodothyronine (T3), thyroxine (T4), and TSH levels of thirteen patients with psychogenic sexual dysfunction and thirteen controls were studied. Patients showed lowered T4 levels in comparison with the control group whereas T3 and TSH levels did not differ significantly. Dexamethasone had a suppressive effect on TSH in patients and in controls while T3 levels were suppressed in the control group only. Patients scored significantly higher on the Hamilton Depression Scale than controls. These results compared with results obtained in patients recovered from major depression might point to endocrinological as well as clinical interrelations between psychogenic sexual dysfunction and minor depression.     

CONGENITAL NEPHROTIC SYNDROME DETECTED BY HYPOTHYROID SCREENING

Abstract. Finnegan, J., Slosberg, E., Postellon, D. and Primack, W. (Borgess Medical Center, Kalamazoo, Michigan and Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, Michigan, USA). Congenital nephrotic syndrome detected by hypothyroid screening. Acta Pediatr Scand, 69: 705, 1980.—An infant was evaluated for a low thyroxine value, detected on routine neonatal screening for congenital hypothyroidism. She was found to have the congenital nephrotic syndrome, and to be euthyroid with low thyroid binding globulin. Congenital nephrosis can be detected by neonatal screening programs which use thyroxine as the primary screening test, but not by those which use TSH. This may be important in those countries in which the incidence of congenital nephrosis approaches that of congenital hypothyroidism.     

EXCEL图表在标记免疫室内质控中的应用

目的探讨Excel图表在标记免疫分析室内质量控制中的应用价值。方法利用OFFICE软件中的Excel图表功能建立游离甲状腺素(free thyroxine,FT4)室内质控图和室内质控参数表,并将每天检测的FT4质控数据输入室内质控参数表中。结果在FT4室内质控参数空表中输入检测数据和日期后,即可看到代表测定值的散点和日期立即出现在控制图中,根据其在室内质控图中的位置可判断测量系统和检测过程是否正常。结论利用Excel图表进行室内质控数据的统计和作质控图,可以克服手工绘制的缺点,提高工作效率,方便查询和回顾性研究,对标记免疫分析质量的提高具有重要意义。     

Screening for thyroid disease and iodine deficiency

The high global prevalence of iodine deficiency and autoimmune thyroid disorders and the mental and physical consequences of these disorders creates a huge human and economic burden that can be prevented, in large part, by early detection and appropriate preventative or therapeutic measures. The availability of sophisticated, sensitive and accurate laboratory testing procedures provides an efficient and effective platform for the application of screening for these disorders. Measurement of urine iodine concentration (UIC) in school children or pregnant women is the recommended indicator for screening populations for iodine deficiency. The severity of the iodine deficiency is classified according to the UIC. Measurement of serum thyrotropin (TSH) as an indicator for population iodine deficiency is used only in neonates and is supplementary to UIC screening. Other indicators such as goitre rates, thyroid function and serum thyroglobulin levels are useful adjunctive but not frontline process indicators. The human and economic benefits of screening for congenital hypothyroidism by measurement of heel-prick TSH have been well documented and justify its universal application. Using this measurement for monitoring population iodine intake is recommended by the World Health Organization but further validation is required before it can be universally recommended. Subclinical thyroid dysfunction is readily detected by current highly sensitive serum TSH assays and its prevalence appears to increase with age, varies with iodine intake and ethnicity and may occur in up to 20% of older age people. Subclinical hyperthyroidism is the less common disorder and screening cannot be justified because of its low prevalence and minimal or insignificant clinical effects. The argument for screening for subclinical hypothyroidism in middle-aged and older women is stronger but lacks evidence of benefit from randomised controlled trials or cost benefit analyses of therapeutic intervention, so it cannot currently be recommended. The publication of recent Clinical Practice Guidelines for management of thyroid disease in pregnancy from the American Endocrine Society and American Thyroid Association provide persuasive arguments for early detection and treatment of overt and subclinical hypothyroidism to prevent obstetric complications and potential neurocognitive disorders in the offspring. Given the indisputable benefits of therapy, the sooner thyroid dysfunction is detected, before or as early as possible in gestation, the more likely there will be a better outcome. Because of the limitations of targeted case detection in women at risk of subclinical hypothyroidism, there has been a gradual shift in opinion to universal TSH screening of all women as soon as practicable in pregnancy. While a positive association exists between the presence of anti-thyroid antibodies and increased pregnancy loss, universal screening of all pregnant women for underlying autoimmune thyroid disease is difficult to justify until there is evidence of beneficial outcomes from randomised controlled trials. Vigorous and liberal targeted case detection remains the recommended strategy to address this problem.     

Arterial hypertension and thyroid disorders: what is important to know in clinical practice?

This review describes the pathogenic mechanisms of blood pressure (BP) regulation and long-term control in thyroid disorders. Variations from the euthyroid status affect virtually all physiological systems but the effects on the cardiovascular system are particularly pronounced. Thyroid disorders induce several hemodynamic changes leading to elevated BP as a consequence of their interaction with endothelial function, vascular reactivity, renal hemodynamic and renin-angiotensin system. However, in thyroid disorders, the regulation of BP and the development and maintenance of variable forms of arterial hypertension (HT) are different. Hyperthyroidism results in an increased endothelium-dependent responsiveness secondary to the shear stress induced by the hyperdynamic circulation, and contributes to reduce vascular resistance. Conversely, hypothyroidism is accompanied by a marked decrease in sensitivity to sympathetic agonists with an increase of peripheral vascular resistance and arterial stiffness. Furthermore in animal models, hypothyroidism reduces the endothelium-dependent and nitric oxide-dependent vasodilatation. HT due to thyroid disorders is usually reversible with achievement of euthyroidism, but in some cases pharmacological treatment for BP control is required. In hyperthyroidism, β-blockers are the first-choice treatment to control BP but when they are contraindicated or not tolerated, ACE-inhibitors or calcium-channel blockers (CCB) are recommended. Hypothyroidism is a typical low rennin HT form showing a better antihypertensive response to CCB and diuretics; indeed in hypothyroidism a low-sodium diet seems further to improve BP control. Randomized clinical trials to compare the efficacy on BP control of the antihypertensive treatment in thyroid disorders are needed.     

Hypothalamic and pituitary function

The thyroid gland is under the control of thyroid-stimulating hormone (TSH) from the pituitary. It secretes thyroxine (T₄) and triiodothyronine (T₃). Iodine is essential for the synthesis of thyroid hormones. T₄ is probably converted to T₃ in peripheral tissues. Thyroid hormones have a role in growth and development, but their principal effect is the control of basal metabolic rate. Deficiency or excess affects all the tissues of the body, reducing or increasing the metabolic rate, resulting in hypothermia or hyperthermia, respectively. Deficiency during development produces mental retardation. Lack of iodine leads to thyroid swelling (goitre) caused by continuing stimulation by TSH. Calcium is one of the most tightly controlled ions in the body; abnormalities can produce muscle paralysis. Bone is the major store of calcium. Calcium reabsorption by the kidney is controlled by parathyroid hormone (PTH) produced by the parathyroid glands, which lie in the posterior part of the lobes of the thyroid gland. PTH secretion is controlled by blood calcium concentrations. Phosphate metabolism is intimately bound up with the control of calcium levels, as is the metabolism of vitamin D, which stimulates the absorption of calcium from the gastrointestinal tract and, in part, from the kidney.     

Exploratory assessment of perfluorinated compounds and human thyroid function

Thyroid hormones play critical roles in human neurodevelopment and adult neurocognitive function. Persistent organohalogen pollutants, such as perfluorinated compounds (PFCs), may interfere with thyroid homeostasis and thus exposures to these compounds might represent risk factors for neurologic and cognitive abnormalities. In this study, serum specimens collected from thirty-one licensed anglers in New York State were analyzed for levels of thyroid stimulating hormone (TSH), free thyroxine (FT₄), perfluorodecanoic acid (PFDA), perfluorononanoic acid (PFNA), perfluoroheptanoic acid (PFHpA), perfluorohexanesulfonate (PFHxS), perfluorooctanoic acid (PFOA), perfluorooctanesulfonate (PFOS), perfluorooctanesulfonamide (PFOSA), and perfluoroundecanoic acid (PFUnDA). PFOS and PFOA occurred in the highest concentrations with geometric means of 19.6 ng/mL (95% CI 16.3-23.5) and 1.3 ng/mL (95% CI 1.2-1.5), respectively. In a cross-sectional analysis, no statistically significant associations were detected for PFCs, or their sum, with TSH or FT₄ at α = 0.05. However, post hoc power analyses, though limited, suggested that moderate increases in sample size, to 86 and 129 subjects, might facilitate 80% power to detect statistically significant associations for FT₄ and PFDA (β = 0.09) and PFUnDA (β = 0.08), respectively. The consumption of sportfish may have contributed to PFDA (r = 0.52, P = 0.003) and PFUnDA (r = 0.40, P = 0.025) levels. This preliminary study does not indicate associations between non-occupational PFCs exposures and thyroid function. However, the possibility for weak associations for FT₄ with PFDA and PFUnDA, PFCs measured in low concentrations, is raised. Given the ubiquity of PFCs in the environment and the importance of thyroid function to neurodevelopmental and neurocognitive endpoints, a confirmatory study is warranted.     

Lower TSH and higher T4 levels are associated with current depressive syndrome in young adults

OBJECTIVE: The relationship of individual thyroid function indices to depression in those without a history of prior thyroid dysfunction is uncertain. METHOD: We examined the relationship between thyroid-stimulating hormone (TSH) and thyroxine (T4) levels and current or lifetime history of depressive symptoms using information from 6869 participants, aged 17-39 years, in the Third National Health and Nutrition Examination Survey without history of thyroid-related illness. RESULTS: We found that lower TSH and higher T4 levels were associated with current depressive syndrome in men, but only higher T4 levels correlated with current depressive syndrome in women. Lifetime depressive syndrome was associated with neither TSH level nor T4 levels in men or women. CONCLUSION: These findings suggest that transient or 'state dependent' changes are associated with depression in those without a history of thyroid illness. Further studies to discern whether these depression-associated changes represent distinct endophenotypes of depression should be encouraged.