Riedel's thyroiditis associated with Hashimoto's thyroiditis.
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Adult↗
Biomedical subjects
G H Daniels
Publications and source records attributed to G H Daniels.
Extra-adrenal pheochromocytoma.
Extra-adrenal pheochromocytomas may arise in any portion of the paraganglion system, although they most commonly occur below the diaphragm. The most common site of occurrence of extra-adrenal pheochromocytoma is the superior para-aortic region between the diaphragm and lower renal poles. Although the traditional teaching has been that 10% of all pheochromocytomas are at extra-adrenal sites, this may be an underestimation. Extra-adrenal pheochromocytomas probably represent at least 15% of adult and 30% of childhood pheochromocytomas. They may be malignant in up to 40% of the cases, although conflicting data add to the uncertainty of this point. Patients with tumors arising at extra-adrenal sites commonly present with headache, palpitations, sweating and hypertension. The diagnosis is most often confirmed by demonstrating increased catecholamine production, usually by measurement of urinary catecholamines and/or their metabolites. CT scanning is presently the imaging procedure of choice for localization. The roles of MRI and 131I-MIBG scintigraphy in the localization process are still being determined. Thorough preoperative pharmacological preparation, attentive intraoperative monitoring and aggressive surgical therapy all have an important role in achieving the safest and most successful outcome. Complete surgical excision is the treatment of choice for primary extra-adrenal pheochromocytoma as well as recurrent or metastatic disease. When residual tumor cannot be resected, medical therapy for symptomatic relief is preferred, since radiotherapy and chemotherapy have limited effectiveness. Extra-adrenal pheochromocytomas are more likely to recur and to metastasize than their adrenal counterparts, making lifelong followup with annual determinations of catecholamine production essential.
Humans↗
The use and limitations of a chemiluminescent thyrotropin assay as a single thyroid function test in an out-patient endocrine clinic.
A chemiluminescent TSH assay (detection limit, less than 0.01 mU/L) allows for accurate measurement of subnormal TSH concentrations. We retrospectively analyzed serum TSH and the free T4 (fT4) index of 460 consecutive endocrine clinic visits to determine the usefulness of TSH measurements alone in the assessment of thyroid function. Additionally, case histories were presented nonconsecutively to one of us (TSH alone or TSH with fT4) to determine if knowledge of the fT4 level would alter management. Of hypothyroid patients on replacement therapy (n = 127), 60% had concordant fT4 and TSH, 14% had subnormal TSH with normal fT4, 18% had high TSH with normal fT4, and 4% normal TSH with high fT4; only 4% were managed differently when the fT4 level was known in addition to TSH. Of the patients receiving suppressive therapy with TSH levels above 0.05 mU/L (n = 81), only 4% were managed differently when fT4 was known; 4% had high fT4. With TSH levels below 0.05 mU/L (n = 64), knowledge of fT4 was felt to be necessary for management in all cases; 53% had high fT4. Twenty-three of 46 (50%) patients being treated for hyperthyroidism had discordant TSH and fT4, including 7 patients with low TSH and low fT4. Two of 21 (10%) patients screened with pituitary/hypothalamic disease had discordant TSH and fT4, and 4 of 9 (44%) patients treated with L-T4 for secondary hypothyroidism had subnormal TSH. Knowledge of fT4 was felt to be necessary in all these cases. We conclude that TSH alone is sufficient for screening and monitoring L-T4 replacement or suppression therapy if TSH levels are above 0.05 mU/L. These patients account for the majority of visits to our endocrine clinic. TSH alone is misleading in pituitary disease and during the treatment of hyperthyroidism. fT4 is needed if TSH levels are less than 0.05 mU/L to assess the degree of hyperthyroidism.
Aged↗
The role of thyroid-stimulating antibodies of Graves' disease in differentiated thyroid cancer.
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Adenocarcinoma↗
Subclinical hyperthyroidism and reduced bone density as a possible result of prolonged suppression of the pituitary-thyroid axis with L-thyroxine.
Spontaneous hyperthyroidism and that due to excessive administration of thyroid hormone result in osteopenia. Bone density was measured in 28 white premenopausal female patients who were taking commonly prescribed suppressive doses of L-thyroxine (mean dose 0.171 +/- 0.035 g) for five or more years. The thyroxine level was 13.5 +/- 2.6 micrograms/dl (normal 8.0 +/- 2.4 micrograms/dl), the free thyroxine index was 4.4 +/- 1.0 (normal 2.4 +/- 0.8), and the triiodothyronine value was 154 +/- 26 ng/dl (normal 132 +/- 32 ng/dl). Basal thyrotropin was undetectable (less than 0.08 microIU/ml) in 23 patients, and thyrotropin measured 20 minutes after thyrotropin-releasing hormone administration was not demonstrable in 13 patients and subnormal in 10 patients. Women who had taken L-thyroxine for 10 or more years (n = 12, age 37 +/- 4 years) had a 9 percent reduction in bone density (0.667 +/- 0.044 g/cm2, p less than 0.01) compared with normal premenopausal age-matched control subjects (n = 56, age 35 +/- 6 years, bone density 0.733 +/- 0.055 g/cm2). It is concluded that prolonged suppressive L-thyroxine treatment may result in mild subclinical hyperthyroidism with adverse effects on bone. Patients requiring suppression of the pituitary-thyroid axis should be given the smallest dose of L-thyroxine necessary to achieve a satisfactory clinical response.
Adult↗
Sonography in the follow-up of 100 patients with thyroid carcinoma.
High-frequency, high-resolution sonography was used to detect recurrent thyroid carcinoma in 73 patients with papillary carcinoma, 16 with medullary carcinoma, 10 with follicular carcinoma, and one with small-cell carcinoma. Of the 36 patients with negative sonograms, 35 had no other evidence of recurrence, while one had surgical proof of recurrence. Of 25 patients with positive sonograms, confirmed with surgery or radioactive iodine (I131) scanning (sonographic sensitivity 96%, specificity 83%), palpation was negative in 17 (palpation sensitivity 32%, specificity 100%). Thirty-two patient with positive sonographic findings had no objective clinical proof of recurrence. There were seven false-positive studies. This study suggests that sonography may be the method of choice for earliest detection and localization of recurrent carcinoma of the thyroid.
Adenocarcinoma↗
Hormonal hyperthermia: endocrinologic causes of fever.
Although hyperthermia is a component of many endocrine diseases, it is uncommon for fever to be the presenting manifestation of hormonal disorders. During a four year period we encountered six patients, hospitalized principally because of fever, who were found to have endocrine causes for the fever. In all, the admitting diagnosis was infection; three were suspected of having tuberculosis, two of gram-negative bacteremia and one of endocarditis. Except for asymptomatic bacteriuria in one patient (who remained febrile despite appropriate antibiotic therapy) infection was ruled out in all cases, and fever was attributed to "masked" thyrotoxicosis, triiodothyronine (T3) toxicosis, subacute thyroiditis, primary adrenal insufficiency, secondary adrenal insufficiency and pheochromocytoma. In a seventh patient, extreme pyrexia developed in the setting of the thyroid storm. The importance of hormonal mechanisms in thermoregulation is discussed.
Addison Disease↗
Alkaline phosphatase isoenzyme patterns in hyperthyroidism.
Fifteen of 36 hyperthyroid patients had elevation in serum alkaline phosphatase activity. There was no difference in mean thyroxine (T4), triiodothyronine (T3), age, or duration of illness between the groups with high alkaline phosphatase and normal alkaline phosphatase levels. After treatment, serum alkaline phosphatase levels rose as T4 levels declined; at 3 months, the mean serum alkaline phosphatase value rose from 7.1 Bodansky units to 10.3 Bodansky units (P less than 0.005), while the mean T4 value fell from 18 microgram/dl to 7.2 microgram/dl (P less than 0.005). In some patients, serum alkaline phosphatase values have remained elevated for more than 1 year, despite continued normality in thyroid variables. Before therapy, isoenzyme patterns analyzed by polyacrylamide gel electrophoresis were qualitatively normal. As therapy was instituted, the isoenzyme patterns changed markedly, with increased amounts of bone alkaline phosphatase appearing in the serum as T4 levels were declining and total alkaline phosphatase was rising. Thyroid tissue homogenates from patients with Graves' disease were found to have very low levels of alkaline phosphatase activity and an isoenzyme pattern quite distinct from that found in the serum.
Adolescent↗
Cyclophosphamide in the management of advanced Graves' ophthalmopathy. A preliminary report.
Three patients with advanced Graves' ophthalmopathy were treated with cyclophosphamide. All had proptosis and diplopia. One patient had disabling iatrogenic Cushing's syndrome from steroid treatment of the ophthalmopathy and had undergone bilateral orbital decompression before cyclophosphamide therapy; steroids could not subsequently be withdrawn. When cyclophosphamide was administered to the cushingoid patient, withdrawal of glucocorticoid therapy was then possible. Diplopia completely resolved in two patients and improved in the third coincident with administration of cyclophosphamide. Deteriorating visual acuity resolved in one patient. Chemosis improved in the two affected patients. Proptosis was unchanged in all three patients. Cyclophosphamide deserves further study as a therapeutic agent in Graves' disease.
Administration, Oral↗
Myocardial function in hypothyroidism. Relation to disease severity and response to treatment.
Systolic time intervals (ST) were used to evaluate myocardial function prospectively in 29 hypothyroid patients. The patients were divided into three categories of disease severity: (1) severe hypothyroidism, (2) mild hypothyroidism, and (3) decreased thyroid reserve or "prehypothyroidism." Groups 1 and 2 showed decreased myocardial contractility with a prolonged preejection period (PEP), shortened left ventricular ejection time (LVET), and increase PEP/LVET, compared with normal controls. The STI were more abnormal (P less than .05) in group 1 than in group 2, suggesting that the severity of myocardial dysfunction correlates with the severity of the hypothyroidism. Group 3 had normal STI. Ten patients were restudied when euthyroid and showed complete normalization of their STI, supporting the thesis that hypothyroidism was the sole cause of the initial myocardial dysfunction.
Female↗
Noninvasive evaluation of cardiac function in hypothyroidism. Response to gradual thyroxine replacement.
Left ventricular performance was studied in 15 patients with severe, primary hypothyroidism (mean serum total thyroxine of 0.8 mug per 100 ml and serum thyrotropin of 160 muU per milliliter). Pretreatment systolic-time intervals were characterized by prolongation of the pre-ejection period (delta PEP = +30) and reduction of the left ventricular ejection period (delta LVET = -23) with a resultant increase in the PEP/LVET ratio (0.47). Nine of 14 patients demonstrated pericardial effusions. These abnormalities were reversed with physiologic thyroxine replacement. Further reductions of the delta PEP and PEP/LVET ratio occurred with supraphysiologic doses (200 to 300 mug per day). During therapy, delta PEP was inversely correlated with serum thyroxine (P less than 0.001) and directly correlated with serum thyrotropin (P less than 0.001). Thus physiologic thyroid hormone replacement, appropriately adjusted to need, appears necessary in hypothyroidism for optimal left ventricular function.
Adult↗
Thyroid function tests during the early phase of subacute thyroiditis.
Six patients with subacute thyroditis were followed with serial measurements of T4, FT4, TSH and RAI uptake. Five of the six underwent TRH stimulation early in the course of their illness. All six patients had elevated or high normal values for T4 and FT4 at the time of their clinical presentation (mean = 13.8 microgram per 100 ml and 3.9 ng per 100 ml, respectively). RAI uptakes were 1% or less in all six. TRH testing revealed a suppressed TSH response (mean deltaTSH less than0.1 muU/ml) in all five patients tested, suggesting hyperthyroidism. After initial studies were performed, five patients were treated with L-triiodothyronine (L-T3) and one with aspirin. All patients improved over a two to four week period of time, no relapses being noted.
Adult↗
The pituitary-thyroid axis in adults with phenylketonuria.
Serum thyroxine and triiodothyronine levels in 15 adult phenylketonuric patients on an unrestricted diet were normal despite reduced circulating tyrosine levels. Serum thyrotropin levels were normal in the basal state or in response to thyrotropin-releasing hormone in selected patients tested. These results support and extend previous observations of normal thyroid function in phenylketonuria.
Adolescent↗
Breast cancer in the Forbes-Albright syndrome.
A 33 year old woman with persistent galactorrhoea developed breast cancer six years after pituitary radiation for a pituitary adenoma (Forbes-Albright syndrome). The possible role of prolactin in human mammary cacinoma is discussed.
Adult↗
Triiodothyronine-induced thyrotoxicosis in ophthalmic Graves disease.
A euthyroid woman with ophthalmic Graves disease developed endogenous hyperthyroidism coincident with T3 suppression test. There is a putative role of liothyronine administration in precipitating or activating hyperthyroidism. Aberrancies in T3 suppression testing in graves disease occur.
Bendroflumethiazide↗
Case report. An autonomously functioning thyroid adenoma in a male with thyroxine-binding globulin excess.
A male with thyroxine-binding globulin (TBG) excess and an autonomously functioning thyroid adenoma is presented. The problem of diagnosing hyperthyroidism in the presence of TBG excess is discussed. The utility of the thyrotropin-releasing hormone test (TRH) is emphasized.
Adenoma↗