1/12. thyrotoxicosis with low serum total T3 level in patients with destructive thyroiditis and non-thyroidal illness. The serum total T3 level, evaluated in 687 patients with thyrotoxicosis diagnosed by an elevated serum free T4 level and suppressed serum TSH level, was found to be high in 98.1% and normal in 1.9% of 592 patients with Graves' hyperthyroidism, and high in 75.8%, normal in 21.1% and low in 3.2% of 95 patients with destructive thyroiditis. Non-thyroidal illness was found in about a third of the patients with thyrotoxicosis and a normal serum total T3 level. The serum total T3 level was low with elevated serum thyroglobulin and reverse T3 levels in three patients with severe non-thyroidal illness, in whom the thyroidal radioactive iodine uptake was suppressed and the thyrotoxicosis resolved spontaneously with a normalization of the serum total T3 level after recovery from the destructive thyroiditis and non-thyroidal illness. It is therefore concluded that thyrotoxicosis with a low serum total T3 level, partially due to associated non-thyroidal illness, is more frequently found in patients with destructive thyroiditis than in those with Graves' hyperthyroidism. ( info) |
2/12. Congenitally enlarged extraocular muscles: can congenital thyroid eye disease exist in a euthyroid infant? A 2-month-old boy presented with hypotropia, eyelid retraction, and proptosis of the left eye. CT and ultrasound demonstrated enlarged extraocular muscles. Both the infant and mother were euthyroid. The patient underwent inferior rectus recession, lower eyelid retractor disinsertion, and entropion repair. biopsy of the inferior rectus and oblique muscles was normal. The clinical presentation and workup appear to be most consistent with thyroid eye disease, which, to our knowledge, would be the first reported case of euthyroid congenital thyroid eye disease with a euthyroid mother. ( info) |
3/12. Artifactual elevation of thyroid-stimulating hormone. A clinically euthyroid patient was found to have a normal serum thyroxine level and an elevated plasma thyrotropin (TSH) level measured by fluoroimmunoassay. Thyroid hormone therapy failed to suppress the TSH level. The TSH level was unresponsive to thyrotropin-releasing hormone (TRH) administration, alpha-subunits of pituitary glycoproteins were undetectable in her plasma, and imaging of the pituitary-hypothalamic region was normal. Measurement of TSH with an assay containing sheep antibody to TSH failed to reveal TSH in the patient's plasma. Addition of mouse IgG to the TSH fluoroimmunoassay reduced the patient's TSH to an undetectable level. These observations are consistent with a spurious elevation of TSH due to the presence of an anti-mouse antibody. Artifactual elevations of TSH have not been identified commonly, but this possibility should be considered when the TSH level is inappropriate for the apparent state of thyroid function. ( info) |
4/12. Elevated thyroxine and free thyroxine in euthyroid patients: familial dysalbuminemic hyperthyroxinemia. An eleven year old male was evaluated because of persistent elevation of thyroxine levels and elevated thyroxine index calculated as "T7" but normal thyrotropin levels. The findings were demonstrated by thyroxine binding protein electrophoresis to be due to aberrant thyroxine binding to albumin. The abnormality was also documented in the patient's father. This entity, known as familial dysalbuminemic hyperthyroxinemia, is being reported with increasing frequency and should be suspected when elevated total thyroxine and free thyroxine or "T7" levels are associated with a normal thyrotropin level. The case reported is somewhat unusual in that the triiodothyronine affinity of the aberrant protein appears to be more pronounced than usually reported with this syndrome and the corresponding total triiodothyronine level was significantly elevated. ( info) |
5/12. 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. ( info) |
| The correct diagnosis of benign hyperthyroxinemia in this patient and his family members will spare them the unnecessary testing and treatment for thyrotoxicosis that has befallen some such patients. Results of the usual blood tests for assessment of thyroid function, such as T4, T3, and thyrotropin determinations, were not uniformly diagnostic, and were potentially misleading. An increased T4 level, a nonsuppressed TSH level, normal levels of FT4 and FT4D, and a low level of T3RU were clues that led to a request for specific measurement of serum TBG levels in multiple family members; family testing was essential for the diagnosis of euthyroid hyperthyroxinemia due to familial hepatic overproduction of TBG. ( info) |
7/12. thyroid function tests in patients with familial dysalbuminaemic hyperthyroxinaemia (FDH). Two patients with familial dysalbuminaemic hyperthyroxinaemia (FDH) are described in whom the albumin variant resulted in raised total T4 levels, and artefactually raised free T4 using a 'single-step' technique employing an analogue of T4 as tracer. The first patient was clinically euthyroid and presented with relapse of schizophrenia and abnormal thyroid function tests (total T4 336 nmol/L, total T3 4.2 nmol/L, TSH 1.8 mU/L, free T4 73 pmol/L). These results led to diagnostic confusion and the patient was treated with a short course of anti-thyroid drugs. The second patient had signs and symptoms of thyrotoxicosis at her first visit but was clinically euthyroid 5 months later when she was 10 weeks pregnant. thyroid function tests were total T4 259 nmol/L, total T3 3.6 nmol/L, TSH 3.8 mU/L, free T4 46 pmol/L. Further studies showed both patients to be biochemically euthyroid. A variant albumin was confirmed in both patients by a screening test for FDH and by reverse-flow electrophoresis. family studies on 10 relatives of the first patient identified eight with FDH. A simple screening procedure for the indentification of FDH is described and the use of laboratory tests in suspected cases is discussed. ( info) |
8/12. Familial dysalbuminemic hyperthyroxinemia associated with primary thyroid disease. This study describes a family with intrinsic thyroid disease in addition to familial dysalbuminemic hyperthyroxinemia, a syndrome associated with euthyroidism and increased binding of thyroxine to serum albumin. The simultaneous occurrence of thyroid disease and elevated serum thyroxine concentrations due to familial dysalbuminemic hyperthyroxinemia may confound the diagnosis of the two concurrent disorders and the subsequent therapy of the thyroid disease. ( info) |
9/12. Abnormal endocrine tests in a hemodialysis patient. A home hemodialysis patient with abnormal thyroid function tests and hyperprolactinemia is presented. Abnormal thyroid tests included low total triiodothyronine and low total thyroxine and free thyroxine; the latter was documented by the use of both RIA and direct dialysis equilibrium techniques. Serum thyroid-stimulating hormone was normal, and the thyroid-stimulating hormone response to thyrotropin-releasing hormone stimulation was in the low-normal range. Serum prolactin was elevated to more than twice the normal level, and the prolactin response to thyrotropin-releasing hormone was also blunted. The interpretation, pathogenesis, physiologic significance, and management of these abnormalities are discussed. ( info) |
10/12. Portal-systemic encephalopathy and hypothalamic hypothyroidism: effect of thyroid hormone on ammonia metabolism. We describe a 53-year-old woman with portal-systemic encephalopathy and altered thyroid function. Endocrinological studies revealed low levels of free thyroid hormone with an inappropriately low level of thyroid-stimulating hormone that responded to bolus injection of thyrotropin-releasing hormone with a normal but somewhat delayed pattern. On the diagnosis of hypothalamic hypothyroidism, she was treated with levothyroxine sodium. Thyroid hormone replacement improved not only the symptoms of hypothyroidism but the hyperammonemia and consciousness disturbance, which suggested a hitherto undescribed possibility that hypothyroidism may be an exacerbation factor of hyperammonemia and portal-systemic encephalopathy. ( info) |