Form Of Hyperthyroidism Research Articles

Effects of Carnitine on Thyroid Hormone Action

By experiments on cells (neurons, hepatocytes, and fibroblasts) that are targets for thyroid hormones and a randomized clinical trial on iatrogenic hyperthyroidism, we validated the concept that L-carnitine is a peripheral antagonist of thyroid hormone action. In particular, L-carnitine inhibits both triiodothyronine (T3) and thyroxine (T4) entry into the cell nuclei. This is relevant because thyroid hormone action is mainly mediated by specific nuclear receptors. In the randomized trial, we showed that 2 and 4 grams per day of oral L-carnitine are capable of reversing hyperthyroid symptoms (and biochemical changes in the hyperthyroid direction) as well as preventing (or minimizing) the appearance of hyperthyroid symptoms (or biochemical changes in the hyperthyroid direction). It is noteworthy that some biochemical parameters (thyrotropin and urine hydroxyproline) were refractory to the L-carnitine inhibition of thyroid hormone action, while osteocalcin changed in the hyperthyroid direction, but with a beneficial end result on bone. A very recent clinical observation proved the usefulness of L-carnitine in the most serious form of hyperthyroidism: thyroid storm. Since hyperthyroidism impoverishes the tissue deposits of carnitine, there is a rationale for using L-carnitine at least in certain clinical settings.

Thyrotoxicosis induced by alpha-interferon therapy in chronic viral hepatitis.

It has been well documented that treatment of chronic hepatitis B and C infection with interferon alpha (IFN-alpha) can lead to the induction of thyroid autoantibodies and hypothyroidism. Thyrotoxicosis, however, is less frequently observed and less well characterized. We reviewed the medical records of patients who developed thyrotoxicosis while receiving IFN-alpha for either chronic hepatitis B or C infection at Westmead Hospital between 1996 and March 2001. Ten patients (four males and six females) were found to have biochemical thyrotoxicosis. The patients could be divided into two groups with different characteristics. The first group consisted of six patients who had clinical manifestations consistent with Graves' disease, with either diffuse uptake in thyroid scintigraphy and/or positive thyroid-stimulating antibodies. They all required prolonged treatment with antithyroid medications. The second group included three patients who had transient thyrotoxicosis, with progression to hypothyroidism after resolution of thyrotoxicosis. Our study suggests that IFN therapy may provoke two different forms of thyrotoxicosis: a Graves' disease picture or a biphasic thyroiditis pattern. The two entities should be differentiated, as they have different implications for treatment.

The Use of Radioactive Iodine in the Management of Hyperthyroidism in Children

Graves' disease is the most common form of hyperthyroidism in childhood. Current treatment options include antithyroid medications, surgery, and radioactive iodine. Medical therapy is generally associated with long-term remission rates of less than 25% and a small risk of serious adverse reactions that include hepatic failure and bone marrow suppression. Total thyroidectomy is associated with very high cure rates and a small risk of hypoparathyroidism and recurrent laryngeal nerve damage. When radioactive iodine is used at appropriate doses, there is a very high cure rate without increased risks of thyroid cancer or genetic damage. Because of the theoretical risk of thyroid cancer after thyroid irradiation in individuals less than 20 years of age, relatively high doses of radioactive iodine should be administered to minimize residual thyroid tissue.

Serum cytokine levels in autoimmune and non-autoimmune hyperthyroid states.

Although the role of interleukin-2 (IL-2) and interferon gamma (gammaIFN) is still poorly understood in hyperthyroid diseases, it is reasonable to assume that these cytokines may be present at higher levels in Graves' disease (GD) than in other primarily non-autoimmune thyroid diseases. In order to look for an easy method to distinguish GD from primarily non-autoimmune causes of hyperthyroidism, we compared 13 healthy individuals with 21 treated and untreated hyperthyroid GD patients and with 19 patients with hyperthyroidism due to other etiologies: 7 cases of multinodular goiter, 5 cases of excessive hormone replacement and 7 cases of amiodarone-associated hyperthyroidism. All patients presented low TSH levels and a dubious clinical thyroid state. We found a good correlation between TSH and serum IL-2 levels (r = 0.56; P<0.01). Serum IL-2 (P<0.01) and gammaIFN (P<0.01) levels were lower in the hyperthyroid group of patients than in control subjects, suggesting a depressed TH1 pattern in the T-cell subset of hyperthyroid patients. GD had normal IL-2 levels, while patients with other forms of thyrotoxicosis presented decreased IL-2 levels (P<0.05). There was no difference between treated and untreated GD patients. We suggest that the direct measurement of serum IL-2 level may help to confirm hyperthyroidism caused by GD.

Surgery for hyperthyroidism

The concept of therapy for hyperthyroidism combines endocrinology, nuclear medicine and surgery. For selection of the treatment of choice, pathophysiology as well as individual aspects are considered. Surgical therapy is mainly concerned with treatment of functional autonomy, Grave's disease and iodine-excess-related hyperthyroidism based on either autonomous or Grave's disease. For each of these three main groups of hyperthyroidism exist differentiated surgical concepts based on the underlying thyroid disease and its course: The various forms of functional autonomy, solitary autonomous nodules, multifocal autonomy or disseminated autonomy are dealt with selective enucleation-resection, functionally and morphologically oriented resection and extensive resection with little remaining thyroid tissue of about 5-6 ml, respectively. For Grave's disease extensive resections with thyroid-tissue remainders of about 2-4 ml or tatal thyroidectomy are established; the latter demonstrating in cases of concomittant endocrine ophthalmopathy the most convincing results. In cases of iodine-related hyperthyroidism the concept of early and radical surgical treatment, following stabilization of the patient in a reasonably short amount of time shows best results and is thus favored. In these cases, contrary to all other forms of hyperthyroidism, establishment of preoperative euthyroid metabolism is not mandatory.

HYPERTHYROIDISM

Hyperthyroidism, or thyrotoxicosis, results when the body's tissues are exposed to excessive levels of thyroid hormone. Hyperthyroidism affects 2% of women but only one-tenth as many men. Graves' disease is the most common form of hyperthyroidism, often occurring in young adults. It is an autoimmune disorder with an important genetic component. Hyperthyroidism's hallmarks include goiter and myriad signs and symptoms related to increased metabolic activity in virtually all body tissues. Increased sensitivity to circulating catecholamines adds to the clinical picture. Diagnosed by patient history, physical examination, and laboratory tests, Graves' disease is treated with antithyroid drugs, radioactive iodine, and/or surgery, plus supportive therapy. A good treatment outcome can be expected; long-term follow-up is indicated.

Gravesʼ disease and other forms of hyperthyroidism in infants and children

Gravesʼ disease and other forms of hyperthyroidism in infants and children

Thyrotoxicosis

Effective therapy for thyrotoxicosis hinges on prompt recognition of the syndrome. When the diagnosis is suspected clinically but is not certain, the free thyroxine index is the most cost-effective test to order initially. The thyroidal radioactive iodine (123I) uptake is measured to differentiate Graves' disease from thyroiditis and other forms of thyrotoxicosis. Definitive therapy includes antithyroid drugs, iodine 131, and surgery. Patient preference has a large role in the final therapeutic choice.

Hyperthyroidism, Inappropriate Plasma TSH and Pituitary Adenoma in Three Patients, Two Receiving Long-term Phenothiazine Therapy

Hypersecretion of TSH by a pituitary adenoma is thought to be a rare form of hyperthyroidism. We describe three such patients, each of whom presented with clinical hyperthyroidism and a diffuse goitre, without eye signs or dermatopathy. Two were receiving long-term phenothiazine, one of these was also acromegalic. Plasma thyroxine, free T4 and tri-iodothyronine were repeatedly raised in each; plasma TSH was grossly elevated in one and inappropriately normal in the other two. Plasma TSH did not rise in response to thyrotrophin-releasing hormone or metoclopramide and was not suppressed by L-dopa in any patient. Anti-thyrotrophin receptor antibodies were undetectable. Skull radiographs showed erosion and expansion of the pituitary fossa and CT scans confirmed a pituitary mass in each patient. A pituitary adenoma was removed by transphenoidal surgery in two patients and a TSH-secreting adenoma was confirmed by immunocytochemical staining and electron microscopy. Both patients were clinically euthyroid post-operatively but still had evidence of TSH excess. Pituitary surgery was technically unsuccessful in the third patient. Although two patients had hyperthyroidism of long duration, all three were diagnosed within one year of the introduction of a sensitive TSH assay to our laboratory. A TSH-secreting pituitary adenoma may be a more common cause of hyperthyroidism than has been believed.

Community outbreak of thyrotoxicosis: Epidemiology, immunogenetic characteristics, and long-term outcome

Between January and March 1984, the first community outbreak of transient thyrotoxicosis in the United States was documented in a seven-county area of southeastern Nebraska; 36 of the total 49 patients resided in York County (2.4 cases per 1,000 population). The median age of patients was 36 years, range six to 82 years; 51 percent were women. By definition, all patients were symptomatic, visited a physician, and had a newly identified elevated serum concentration of thyroxine or triiodothyronine of unknown cause. None had a goiter or a painful thyroid gland. Low 131I uptake measurements were found in all nine patients studied. Six patients were hospitalized; none died. Investigation of all 12 household contacts of eight selected patients revealed five additional persons with thyrotoxicosis and four with asymptomatic hyperthyroxinemia. A case-control study revealed that illness was associated with a significantly higher frequency of a reported recent respiratory viral-like condition. In another case-control study, the HLA-DR3 antigen was present in more case subjects (39 percent) than control subjects (14 percent). In addition, a significantly higher proportion of patients than control subjects purchased beef from one of the three supermarkets in York Country. Concomitant with the outbreak, the supermarket implicated in the outbreak purchased an unusually large quantity of beef (7,000 pounds) from a nonregular supplier in Nebraska, which had reportedly instituted the practice of trimming gullets (a procedure that removes the muscles from bovine larynx for beef) about three months earlier. Thus, it is concluded that the Nebraska outbreak, like one in Minnesota that occurred 18 months later, probably resulted from patients having eaten ground beef that was contaminated with bovine thyroid gland. This form of thyrotoxicosis, perhaps misdiagnosed as painless thyroiditis in the past, probably represents a previously under-recognized public health problem.

Status asthmaticus associated with hyperthyroidism.

The syndrome of asthma and hyperthyroidism is uncommon and has been reported to occur approximately once every three hundred admissions for asthma. The frequency may be higher with an increased awareness; however, when this syndrome is present, it is usually associated with a very severe form of asthma necessitating frequent emergency treatment and hospitalization. Although severe asthma alone or together with side effects of drugs used in its treatment may mimic many symptoms associated with hyperthyroidism, an awareness of this syndrome will enable one to easily establish the diagnosis. In these cases, the hyperthyroidism may be iodide induced especially in those patients with diffuse or nodule thyroid goiter. Since this form of hyperthyroidism may be self-limiting, initial treatment should include a trial of propylthiouracil or methimazole up to six months. Medical therapy of the hyperthyroid results in dramatic improvement of the asthma.

The Clinical and Thyroid Function Studies of Lymphocytic Thyroiditis with Spontaneously Resolving Hyperthyroidism: Comparison to Subacute Thyroiditis

Lymphocytic thyroiditis with spontaneously resolving hyperthyroidism (LT-SRH) has been reported in the past years, and is referred to as “silent thyroiditis.” It is characterized by a low or decreased radioactive iodine uptake (RAIU) of thyroid in a patient with hyperthyroidism in whom initial diagnosis is generally thought to be Graves’ disease.Thirty-five patients who had hyperthyroidism or goiter with decreased RAIU have been assessed. Twenty-four (68.6%) of 35 patients had LT-SRH and the remaining patients, subacute thyroiditis (SAT).The clinical characteristics of the patients with LT-SRH were a history of delivery, painless goiter, elevated T3 and T4 levels and positive anti-microsomal antibodies. Anti-microsomal antibodies were positive in 70.8% of the LT-SRH group, whereas 12.5% in the SAT group. Resolution of the hyperthyroidism took 8 to 12 months.It is considered that LT-SRH is an autoimmune thyroiditis with spontaneously resolving hyperthyroidism and determination of the RAIU is very useful in differentiating from other forms of hyperthyroidism.

Thyroid stimulating immunoglobulins: measurement and clinical use.

Graves’ disease is the commonest form of hyperthyroidism in which excessive production of thyroid hormones by the hyperplastic overactive thyroid gland produces elevated serum levels of the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4). Many of the manifestations of Graves’ disease, increased basal metabolic rate, increased heart rate, heat intolerance, sweating and nervousness, can be attributed to the peripheral actions of the excess thyroid hormones. The pathogenesis of many of the other dramatic features of Graves’ disease, such as the eye involvement or localized skin changes, is not fully understood, but circulating immunoglobulins with thyroid stimulating activity are almost certainly linked to excess thyroid hormone production and thereby cause the hyperthyroidism.

Rare hyper-, hypothyroid states require unconventional therapies

Once upon a time there were hyperthyroidism and hypothyroidism. Therapy for the first aimed at diminishing excess hormone production, while therapy for the second aimed at replacing it. But now research from a variety of laboratories suggests that in certain conditions these therapeutic approaches, however logical on the surface, may be unnecessary and even dangerous. Some of these relatively rare conditions were discussed at the Seventh International Congress of Endocrinology in Quebec City and at the annual meeting of the American Thyroid Association in New York City. The recurrent message was: Hyperthyroidism is not always hyperthyroidism. And the same holds true for hypothyroidism. For example, at the endocrinology meeting, held last summer, Thomas F. Nikolai, MD, discussed a condition noticed at the Marshfield (Wis) Clinic and regarded as a clinically new form of hyperthyroidism not recognized before 1970. Called "silent thyroiditis" (or lymphocytic thyroiditis with spontaneously resolving hyperthyroidism), this disease

Iodide excess and thyroid function.

Editorials1 March 1983Iodide Excess and Thyroid FunctionIRWIN KLEIN, M.D., GERALD S. LEVEY, M.D.IRWIN KLEIN, M.D.Search for more papers by this author, GERALD S. LEVEY, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-98-3-406 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptAlthough the critical role of iodine in the regulation of thyroid gland function has been recognized for many years, other aspects of its use remain controversial. The appropriate amount of iodine needed for supplementation of food and water supplies, the role of iodine in the treatment of persons in the area of a nuclear reactor accident or patients with Graves' disease, and the incidence of iodide-induced thyrotoxicosis in the general population have all been debated. Thus, the recently published review, "Iodide-Induced Thyrotoxicosis" by Fradkin and Wolff (1), is timely.Iodide-induced thyrotoxicosis is a form of hyperthyroidism that generally effects an...

Pitfalls in the Laboratory Diagnosis of Atypical Hyperthyroidism

When hyperthyroidism results from active thyroidal secretion, both serum hormonal levels and the radioactive iodine uptake (RAI) are elevated. Discordant results (increased serum hormone levels and a low RAI) are found either in the usual forms of hyperthyroidism when large quantities of iodide are ingested, or in atypical forms of hyperthyroidism, including spontaneously resolving hyperthyroidism of subacute thyroiditis, thyrotoxicosis factitia, toxic struma ovarii, and functioning metastatic thyroid cancer. Two patients are described who exemplify pitfalls in the interpretation of thyroid function test results in atypical hyperthyroidism. The following guidelines are helpful in avoiding these pitfalls: (1) An RAI should be performed in all thyrotoxic patients to confirm the presence of thyroidal hypersecretion, rather than atypical hyperthyroidism. (2) A positive response to thyroid-stimulating hormone stimulation is an important finding differentiating the other atypical forms of hyperthyroidism listed from subacute thyroiditis.

Painless Thyroiditis as a Cause of Hyperthyroidism

In the past three years, reports of 39 patients (17 male, 22 female) with an unconventional form of thyroiditis who had signs and symptoms of hyperthyroidism, low to absent thyroidal uptake of radioactive iodine (¹³¹I) and no history of thyroidal pain and/or tenderness have appeared in the literature^1-7and in this issue of theArchives(p 45). This form of hyperthyroidism has accounted for 3.6%⁶to 16%⁷of all cases of thyrotoxicosis and for 29% of thyroiditis.⁶Although this virtual epidemic of reports suggests a new disease entity,⁸painless thyroiditis has been recognized for the past 20 years.⁹ The hyperthyroidism may be mild or very severe. The thyroid gland is nontender, firm, and (usually but not always⁷) mildly to moderately enlarged. As expected, exophthalmus is absent, but the eye signs associated with increased sympathetic tone may be present. The hyperthyroid phase lasts

The occurrence of T3 thyrotoxicosis in pregancy.

A case of T3 thyrotoxicosis in pregnancy is described. The condition may be overlooked if serum T3 levels are not measured routinely since the usual tests of thyroid function are unaltered in this form of hyperthyroidism.

Plasma thyrotrophin levels in thyroid disease and effect of treatment.

ABSTRACT A radioimmunoassay has been developed and was applied in a first study to the determinations of human plasma TSH in normal subjects. In the present work a systematic study was made of the relation between the pituitary and the thyroid gland in thyroid disease, and on the effect of various forms of treatment in 750 patients. Normal values for adults of both sexes were found to be 0.19 mU/ml, referred to the international bovine TSH standard (USP). No TSH was found in pituitary hypothyroidism. Elevated levels, up to fifteen times those of normal subjects, were found in myxoedema. The low initial values in all forms of thyrotoxicosis were followed by modifications during treatment depending on the kind of treatment used. Every qualitative or quantitative deficiency of thyroid hormone secretion was accompanied by an elevation of TSH (euthyroid nodular goitre, thyroid carcinoma, subacute thyroiditis and Hashimoto's disease) and treatment with thyroid hormones induced a rapid fall in plasma TSH. The action of lysine vasopressin was also studied.

Long-term results of the effect of radioactive iodine-131 therapy in patients with thyrotoxicosis on the content of acetone bodies in the blood

From 1955 to 1958 inclusively, we studied the content of acetone bodies in the blood of 56 patients with thyrotoxicosis treated with radioactive iodine-131 with a half-life of 8 days. The function of the thyroid gland in all patients was increased to one degree or another. We have established an increase, up to significant, in the level of acetone bodies in the blood in 24 out of 25 patients with a severe form of thyrotoxicosis and in most cases with an average form.