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PubMed2005

[A family with familial dysalbuminaemic hyperthyroxinaemia].

OBJECTIVE: To report a family of familial dysalbuminaemic hyperthyroxinaemia(FDH). METHODS: Four members, including the female proband, mother, daughter and brother, went through the measurement of thyroid hormone and thyroid-stimulating hormone (TSH). Electrophoretic analysis of the patient's serum proteins was carried out after the patient's serum being incubated with fluorescein isothiocyanate (FITC) labeled thyroxine(T4), The point mutation of Alb gene was determined in all members. RESULTS: The measurements of thyroid hormane and TSH showed that in three members (the proband, her mother and her daughter), the total thyroxine(TT4) serum level was high, the total triiodothyronine(TT3), FT4, FT3 and TSH serum levels were normal. And the enhanced albumin binding of fluorescenced T4 by electrophoresis showed a mutation transition 653 G-->A on DNA coding region of albumin. But in the proband's brother, the thyroid function and the results of electrophoresis of thyroxine-binding protein and determination of albumin gene were normal. CONCLUSION: A family with FDH in China is firstly reported here, a mutation at albumin gene DNA coding region 653G-->A causing enhanced albumin binding of T4 results in high T4 level.

Adult↗
PubMed1991

Audit of hyperthyroxinaemia and thyrotoxicosis using a sensitive TSH assay.

The aim of this study was determine (a) the causes of hyperthyroxinaemia and (b) the biochemical profile of thyrotoxicosis in a general hospital laboratory for one year using a sensitive TSH assay. Total T4 (TT4) and TSH were measured in all 8,382 samples and TT3, free T4, free T3 and thyroxine binding globulin (TBG) in selected cases. TT4 was elevated in 215 (2.6%). 159 (74%) were due to thyrotoxicosis; 41 (19%) to elevated TBG and 15 (7%) non-thyroidal illness. Thyrotoxicosis (serum TSH less than 0.15m U/1) occurred in 223 (2.7%) of all patients and was diagnosed with high TT4 in 159 (71%), normal due to intercurrent illness. 352 (4%) patients had suppressed TSH while all thyroid hormone values were normal. Thus TT4 may be elevated from causes other than thyrotoxicosis sufficiently frequently to necessitate routine TSH measurements. While Normal TSH measurements nearly always excludes thyrotoxicosis, suppressed values are insufficient to establish a diagnosis or monitor thyroxine replacement therapy.

Humans↗
PubMed1990

Tests of thyroid function: update in the diagnosis and management of thyroid disease.

Current thyroid function tests give the clinician powerful tools for the accurate assessment of thyroid status in the majority of patients encountered. There are, however, a small number of clinical situations in which there appear to be inconsistencies in the interrelationship of the thyroid function tests and/or in which they are apparently inappropriate to the clinical status of the patient. In most instances, there is a rational explanation for these observed alterations. The application of this information should allow clinicians to further refine their diagnostic accuracy and thereby enable them to proceed with an appropriate therapeutic or management program.

Adult↗
PubMed1989

Abnormal thyroid function in hyperemesis gravidarum.

Thyroid function was evaluated in 41 consecutive women with hyperemesis gravidarum (HG). In 11, increased free thyroxin concentrations (FT4) were measured. After one week of conservative therapy, 4 patients with persistent emesis were treated with antithyroid agents. Three of these 4 displayed other signs of hyperthyroidism. Emesis resolved in the other 7 patients within a week of conservative therapy. FT4 levels also returned to normal in these 7 patients within several weeks. Thyrotropin-releasing hormone (TRH) was administered to 10 of the 11 patients. Abnormal TSH responses, suggesting varying degrees of autonomous thyroid function were noted in all 4 patients treated with antithyroid drugs and in 3 of the untreated patients. Underlying clinical signs and symptoms of hyperthyroidism should be sought in patients with HG. In the presence of persistent emesis, despite conservative therapy of at least one week's duration and the presence of abnormal thyroid function studies, the use of antithyroid agents should be considered.

Adult↗
PubMed1989

[Changes in aldosterone and cortisol secretion and serum thyroxine levels in patients with active urolithiasis].

The changes in calcemia and calciuria levels following low calcium diet have been studied in 35 patients with active urolithiasis and in 20 healthy subjects. Blood serum concentrations of thyroxine, cortisol and aldosterone in basal conditions as well as cortisol and aldosterone following stimulation with synacten were determined in addition. The levels of calcemia and calciuria (2.56 +/- 0.015 mmol/l and 4.70 +/- 0.41 mmol/10 mmoles of creatinine, respectively) were found to be significantly higher in patients with active urolithiasis than in healthy subjects. In addition, in patients with urolithiasis the basal blood serum concentrations of thyroxine and aldosterone were significantly higher than in healthy subjects, while the reactivity of cortisol and aldosterone secretion to synacten stimulation was normal. The results obtained suggest the participation of the described hormonal aberrations in the pathogenesis of active urolithiasis.

Adrenal Cortex↗
PubMed1989

Euthyroid hyperthyroxinaemia due to endogenous antibodies to thyroxine and tri-iodothyronine. A case report.

A case of euthyroid hyperthyroxinaemia caused by auto-antibodies to thyroxine and tri-iodothyronine is presented. Gel filtration chromatography of the patient's serum showed increased binding of radio-labelled thyroxine analogue to a macromolecular component, which migrated in the gammaglobulin region on electrophoresis. Precipitation by protein A confirmed that this was an immunoglobulin. The importance of recognising this condition so that inappropriate therapy can be avoided is stressed.

Autoantibodies↗
PubMed1986

Diagnostic value of free triiodothyronine in serum.

Serum free T3 concentration has been assessed in various thyroid conditions by a T3 analog method and the results compared with those obtained by equilibrium dialysis in the same individuals. The methodology is easy to perform and reproducible. FT3 determination appears to be especially valuable in detecting borderline thyrotoxicosis as in cases previously cured from thyrotoxicosis but suspected of relapse, or in nontoxic goitrous patients overtreated with T4.

Evaluation Studies as Topic↗
PubMed1988

Familial generalised resistance to thyroxine: case study.

We describe the clinical features of members of a family with an atypical form of thyroid hormone resistance syndrome, affecting thyroxine predominantly. Relevant diagnostic clinical and biochemical investigations are outlined and discussed.

Adolescent↗
PubMed1987

Elevation of free thyroxine measurements in patients without thyrotoxicosis.

The recent development of single step analogue assay techniques to measure free thyroxine in serum has meant that this estimation has become widely used as a first line test of thyroid function. However these assays are subject to in-vitro interference in two ways: where there is a variant serum albumin in familial dysalbuminaemic hyperthyroxinaemia, or where there are circulating thyroid hormone binding antibodies. In both these situations a spuriously high result for free thyroxine is obtained. This may have serious implications for patient management and we describe 10 patients in whom the finding of a misleadingly high free thyroxine concentration led to confusion in diagnosis and, in eight of the 10, to inappropriate antithyroid treatment. Clinicians should be aware of these technical problems and where a result for the free thyroxine concentration seems inappropriate to the patient's clinical state then measurement of thyrotrophin (TSH) by a sensitive immunometric method should be performed. If the results remain confusing the presence of a variant serum albumin or thyroid hormone binding antibodies should be sought.

Adult↗
PubMed1994

Thyroxine excess and pregnancy.

Pregnancy is characterised by a physiological increase in bound thyroxine but normal values of free hormone. Human chorionic gonadotrophin (hCG may stimulate the thyroid to produce hyperemesis gravidarum (with mild to moderate hyperthyroidism) or result in high thyroid hormone levels associated with gestational trophoblastic disease. Hyperthyroidism occurring during pregnancy is usually due to Graves' disease and must be treated to prevent congenital anomalies, low birth weight and premature labour. Thionamide drugs should be used with a preference for propylthiouracil (PTU) and continued in low doses up to labour. Breast feeding is possible in patients on low dose PTU. In the management of hypothyroidism during pregnancy thyroxine dose may require to be increased but excess dosage should be avoided because of its unwanted effects on foetal cerebral maturation. Neonatal hyperthyroidism due to transplacental passage of thyroid stimulating antibodies (TsAb) should be checked for in pregnant patients with autoimmune thyroid disease. As antithyroid drugs cross the placenta they may be used as therapy in this condition. Prevention of neonatal goitre is vital. Postpartum development of hyperthyroidism may be due to an exacerbation of pre-existing Graves' disease, development of new Graves' hyperthyroidism or postpartum thyroiditis with transient hyperthyroidism. Differentiation by measurement of TsAb and thyroidal iodine uptake is important because of therapeutic considerations.

Antithyroid Agents↗
PubMed1994

Effects of thyroxine excess on peripheral organs.

Aim of this paper is to review the effects of T4 excess due to exogenous thyroid hormone administration on target organs, with particular regard to heart, bone, liver and pituitary. Therapy with TSH-suppressive doses of T4 has been shown in a cross sectional echocardiographic study to increase left ventricular contractility and to induce mild myocardial hypertrophy. Whether the latter represents a risk for the patients remains a matter of debate. Clinically it does not seem to be important. The long-term evaluation of T4-therapy has provided controversial results. Some have reported that T4-treated patients under the age of 65 have an increased risk of ischemic heart disease, whereas others were unable to find any change in morbidity, mortality and quality of life, including cardiovascular events. Thyroid hormones enhance both osteoblastic and osteoclastic activities in cortical and trabecular bone. Overt hyperthyroidism is well known to represent a risk factor for osteoporosis. Studies in the late eighties have suggested a reduced bone density in T4-treated patients, with a particular risk for cortical bone in postmenopausal women. More recent studies have failed to show any substantial T4-related change in bone mass. Taken together the evidence of the literature suggests that TSH-suppressive therapy with T4 is, if well controlled, probably not associated with significant loss of bone mass at least in premenopausal women. A mild elevation of the activity of hepatic enzymes (glutathione-S-transferase, gamma glutamyltransferase, alanine amino-transferase, angiotensin-converting enzyme) has been observed in patients under T4 treatment in TSH-suppressive doses.(ABSTRACT TRUNCATED AT 250 WORDS)

Bone and Bones↗