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PubMed1989

A newer avenue for evaluation of thyroid dysfunction.

Attempt has been made to rationalise the biochemical assessment of patients suspected to have thyroid dysfunction by introduction of a new rapid and supersensitive immunoradiometric assay (IRMA) for TSH. 294 patients were subjected to thyroid investigation viz; tT3, tT4 and TSH (IRMA). Of these, 51 (17.34%) were hypothyroid, 22 (7.48%) were hyperthyroid and 221 (75.1%) were euthyroid. The ratio of thyroid disorder in male to female was 1:3.38. In all patients with hyperthyroidism TSH (IRMA) was 0.05 to undetectable and it was more than 4.5 ulu/ml in hypothyroid patients. TSH (IRMA) was low in one euthyroid patient a 0.34% incidence of false negativity. In 2 patients with subclinical hyperthyroidism TSH (IRMA) was low while tT3 and tT4 were normal. TSH (IRMA) therefore may obviate the need for more time consuming and expensive TRH test and simplify the approach to thyroid function tests in patients suspected to have masked or overt hyperthyroidism.

Adolescent↗
PubMed1984

A case of untreated chronic goitrous autoimmune thyroiditis with spontaneous fluctuation between different metabolic levels.

Documented thyrotoxicosis developed in a 12 year old girl with chronic autoimmune thyroiditis. During the following 3 years there was a spontaneous progression from hyperthyroidism to hypothyroidism and vice versa fluctuating from one metabolic state to another. The diagnosis of Hashimoto's thyroiditis was based upon thyroid function tests, elevated titres of antibodies against thyroid constituents, and upon thin-needle biopsy of the enlarged thyroid gland.

Autoimmune Diseases↗
PubMed1990

Review: thyroid function in psychiatric illness.

The development of highly sensitive immunometric assays for thyroid-stimulating hormone (TSH) has provided increased understanding of thyroid hormone regulation but, paradoxically, has contributed to a kaleidoscopic complexity of thyroid function test variability in hospitalized patients with nonthyroidal illness (NTI). In primary hypothyroidism, an elevated TSH is the most sensitive chemical index available, although early cases may show a hyperresponse of TSH to thyrotropin-releasing hormone (TRH) stimulation when the TSH is still within the normal range. The ability of the new TSH assays to discriminate between normal and low levels now allows the diagnosis of thyrotoxicosis to be confirmed by a suppressed TSH in the presence of elevated serum thyroxine (T4) and/or triiodothyronine (T3). The TRH stimulation test is virtually obsolete for the diagnosis of thyrotoxicosis but remains of much interest in the investigation of psychiatric syndromes. Approximately 25% of patients with depression have a blunted TSH response (a rise of less than 5 microU/mL) that differs from thyrotoxicosis, wherein the TSH response is suppressed under 1 microU/mL. The cause of the blunted TSH is uncertain but is not due to hyperthyroidism. In contrast, close to 15% may have a TSH hyperresponse to TRH and/or elevated antithyroid antibodies. Thyroid hormone treatment may benefit the depression in some of these cases. In the sick thyroid state of nonthyroidal illness, a low T3 level is the initial manifestation. In more severe cases, the T4 also falls, the free T4 level in this situation is variable, both normal and low levels being reported from different laboratories. A diagnosis of hypothyroidism requiring treatment with thyroid hormone therapy is unlikely unless there is a concomitant lowfree T4 and elevated TSH in a patient who is not in the process of recovery. In acute psychiatric admissions, there is a high frequency of hyperthyroxinemia. The TSH in these cases is generally either normal or high, suggesting central activation of the hypothalamic-pituitary-thyroid axis. In most instances, the thyroid function tests normalize within 2 weeks, and treatment directed toward the thyroid gland is not indicated. Suppressed TSH levels, usually associated with a normal free T4, has also been described in such patients. Finally, various medications utilized in psychiatric practice have diverse effects on thyroid function and can cause diagnostic difficulty. These include lithium, phenytoin sodium, and carbamazepine, and their effects are reviewed.

Diagnosis, Differential↗
PubMed2004

Diagnosis and management of thyroid disease and the critically ill patient.

OBJECTIVE: To review current concepts in the diagnosis and management of thyroid disease in the critically ill patient. DATA SOURCES: A review of articles reported on thyroid disease and the acutely ill patient. SUMMARY OF REVIEW: Normal thyroid function depends on an integrated response between the pituitary and thyroid gland to provide an appropriate circulating T4 level which is converted to T3 by peripheral tissues. Thyroid hormone increases oxygen consumption and regulates lipid and carbohydrate metabolism and normal growth and maturation of tissues. In patients with a severe non-thyroidal illness, the thyroid stimulating hormone (TSH), free thyroxine (FT4) and free 3,5,3-triiodo-L-thyronine (FT3) levels decrease. Dopamine, dobutamine or corticosteroid therapy may also reduce TSH levels. The TSH and T4 levels often return to low normal levels, although with continued severe illness they may remain low. The clinically euthyroid state is maintained in the presence of a reduction in FT3 levels partly due to an increase in synthesis of tissues T3 receptors. During the recovery phase of the illness, there is often a transient elevation in the TSH level until the FT4 and FT3 levels are returned to normal. There are no clinical data that have shown a consistent reduction in mortality with thyroid hormone treatment in the critically ill patient. In general, in the absence of clinical signs of thyroid disease, abnormal thyroid function tests should not be treated in the critically ill patient and thyroid function studies should be repeated after the acute illness has resolved. Hypothyroid and hyperthyroid states may present with acute cardiorespiratory failure. Treatment that includes cardiorespiratory resuscitation and thyroid hormone replacement in hypothyroid states and beta adrenergic blockers in hyperthyroid states will often allow correction of the underlying disorder to be achieved successfully. CONCLUSIONS: Abnormal thyroid function tests are commonly found in the critically ill patient and do not require treatment. However, hypothyroid and hyperthyroid states may present with acute cardiorespiratory failure and require careful and specific management strategies to resolve the thyroid disorder.

Journal Article↗
PubMed2001

Hypothalamus-hypophysis-thyroid axis, triiodothyronine and antithyroid antibodies in patients with primary and secondary Sjögren's syndrome.

It has been well established that, anti-thyroglobulin antibodies (ATG) and anti-microsomal antibodies (AMC) may be present in various thyroid disorders and other systemic autoimmune diseases, including Sjögren's syndrome (SS). However, presence of circulating autoantibodies to thyroid hormones, i.e. both to triiodothyronine (T3) and tetraiodothyronine (T4), has not been studied extensively in SS. Autoantibodies to T3 and T4 are very important, because serum T3 and T4 levels may be detected spuriously higher or lower, due to the presence of these autoantibodies. Their presence should be suspected when measured serum thyroid hormone levels are not consistent with clinical status of the patient. SS is a slowly progressive, inflammatory autoimmune disease, affecting primarily the exocrine glands. Thyroid gland, being a target in some autoimmune diseases, is well known to be affected in SS as well. Keeping this possibility in mind, we investigated T3 autoantibody levels and thyroid gland involvement in patients with SS. Twenty-six SS patients (F/M:22/4) with a mean age of 46.6 years, were recruited in this study. Twelve of them were accepted as primary SS (pSS), while others had secondary SS (sSS) (7 with rheumatoid arthritis (RA), 3 with systemic lupus erythematosus (SLE), 3 with progressive systemic sclerosis (PSS) and 1 with sarcoidosis). Thyroid function tests, including T3, T4, fT3, fT4, TSH, ATG, AMC, T3 antibody measurements, thyroid scintigraphy, thyroid ultrasonography and TRH stimulation tests were performed in all patients. We compared our results with those of the twenty healthy normal controls. Serum ATG and/or AMC were detected in three patients with pSS (25%) and no patients with sSS. No significant difference could be shown in the other parameters, including T3 autoantibodies and thyroid function tests. TRH stimulation test was also normal, showing that the hypothalamus-hypophysis-thyroid axis was not affected in patients both with pSS and sSS. In conclusion, we found that T3 autoantibody levels in pSS, were not significantly higher than sSS and normal controls.

Adult↗
PubMed1998

Genetic and biochemical screening for endocrine disease: III. Costs and logistics.

The cost of screening tests in endocrine disease can be determined in a number of ways, including the charge or billed cost, the production cost, or most appropriately the cost to achieve the intended aim of the test (cost-effectiveness). Cost-effectiveness analysis allows clinicians to determine whether an added benefit of a test comes at an acceptable cost. For example, analysis of the cost-effectiveness of routine thyroid function tests prior to surgery in elderly patients with nodular thyroid disease shows that the cost per life saved is only US $405, making the tests clearly cost-effective. Cost-effectiveness does not always equate with affordability, however, especially in developing countries. Thyroid function testing prior to surgery represents only 0.8% of the average household income in Australia and is therefore both cost-effective and affordable, whereas in Sri Lanka the same screening test represents up to 50% of the average monthly income. A survey of membership of the International Association of Endocrine Surgeons worldwide showed that molecular genetic screening for endocrine disease is readily available in 67% of institutions, with all of those having facilities for the rearrangement during transfection (RET) proto-oncogene testing, and lesser numbers having access to the Menin gene, the von Hippel-Lindau syndrome (VHL) gene, or linkage analysis for familial pheochromocytoma. The median cost of screening for the RET proto-oncogene was $290 (range $100-3000). Cost-effectiveness analysis of molecular genetic screening for MEN-II syndrome demonstrates that the cost per life saved is only $5175. This compares favorably with reliance on screening based on annual pentagastrin testing, where the cost per life saved is as high as $76,315. Molecular genetic screening for endocrine disease (e.g., the MEN-II syndrome) is not only cost-effective but the therapy required (total thyroidectomy) is both acceptable and well tolerated.

Cost-Benefit Analysis↗
PubMed2002

Narrow individual variations in serum T(4) and T(3) in normal subjects: a clue to the understanding of subclinical thyroid disease.

High individuality causes laboratory reference ranges to be insensitive to changes in test results that are significant for the individual. We undertook a longitudinal study of variation in thyroid function tests in 16 healthy men with monthly sampling for 12 months using standard procedures. We measured serum T(4), T(3), free T(4) index, and TSH. All individuals had different variations of thyroid function tests (P < 0.001 for all variables) around individual mean values (set points) (P < 0.001 for all variables). The width of the individual 95% confidence intervals were approximately half that of the group for all variables. Accordingly, the index of individuality was low: T(4) = 0.58; T(3) = 0.54; free T(4) index = 0.59; TSH = 0.49. One test result described the individual set point with a precision of +/- 25% for T(4), T(3), free T(4) index, and +/- 50% for TSH. The differences required to be 95% confident of significant changes in repeated testing were (average, range): T(4) = 28, 11-62 nmol/liter; T(3) = 0.55, 0.3--0.9 nmol/liter; free T4 index = 33, 15-61 nmol/liter; TSH = 0.75, 0.2-1.6 mU/liter. Our data indicate that each individual had a unique thyroid function. The individual reference ranges for test results were narrow, compared with group reference ranges used to develop laboratory reference ranges. Accordingly, a test result within laboratory reference limits is not necessarily normal for an individual. Because serum TSH responds with logarithmically amplified variation to minor changes in serum T(4) and T(3), abnormal serum TSH may indicate that serum T(4) and T(3) are not normal for an individual. A condition with abnormal serum TSH but with serum T(4) and T(3) within laboratory reference ranges is labeled subclinical thyroid disease. Our data indicate that the distinction between subclinical and overt thyroid disease (abnormal serum TSH and abnormal T(4) and/or T(3)) is somewhat arbitrary. For the same degree of thyroid function abnormality, the diagnosis depends to a considerable extent on the position of the patient's normal set point for T(4) and T(3) within the laboratory reference range.

Adult↗
PubMed1988

Symptom rating scale for assessing hyperthyroidism.

A hyperthyroid symptom scale (HSS) was designed and administered to ten subjects with untreated Graves' disease. All subjects had clinical and chemical evidence of hyperthyroidism and reproducible HSS scores of 20 or more points. During sequential treatments with propranolol hydrochloride (phase 2) followed by propylthiouracil (phase 3) there was a significant decline in the HSS scores at each phase. Accompanying the decrease in HSS scores was a decrease in heart rate, but there was no change in thyroid function test results at phase 2 and a decrease in heart rate, thyroid function test results, and goiter size at phase 3. This new scale includes ten categories of symptoms, it is sensitive to changes in both the adrenergic and metabolic components of hyperthyroidism, and it is useful in the clinical assessment and management of patients with thyrotoxicosis.

Adult↗
PubMed1983

Antemortem chemical hypothyroxinemia.

Based on reports of hypothyroidism in intensive care unit patients, a preliminary study was instituted in which 40 patients coming to autopsy, with no history of thyroid disease, were studied to include gross and microscopic study of the thyroid gland and the performance of thyroid function tests on all serum specimens submitted within seven days of death. Initial studies show that with the exception of sudden cardiac death, all of the autopsy patients showed evidence of chemical hypothyroxinemia within three days preceding death without any histologic abnormalities of the thyroid gland. Thyroid function tests were subsequently studied of decedents and survivor controls matched for age, sex, disease, and stage of disease if applicable. The findings were similar.

Critical Care↗