Thyroid Crisis
Methimazole
Antithyroid Agents
Hyperthyroidism
Propylthiouracil
Thyroid Gland
Hypoglycemic coma masquerading thyrotoxic storm. (1/33)
A 59-year-old woman was hospitalized in hypoglycemic coma. Although hypoglycemia was promptly reversed, she was in a somnolent, restless state with tachycardia, tremor, profuse sweating, and high body temperature. Thyrotoxic storm was highly suspected and vigorous antithyroid regimens gradually brought her up to normal mental and cardiovascular states in several days. However, profound generalized myopathy necessitated the maintenance with a respirator. One month later, an episode of angina pectoris was followed by generalized convulsion, coma, and death in a few days. Neuroimaging study disclosed posterior leukoencephalopathy syndrome. This case is instructive in that hypoglycemic coma may masquerade the major symptomatology of thyrotoxic storm, and that profound myopathy and angiopathic or angiospastic processes of the brain and the heart may interfere with the outcome. (+info)Gestational thyrotoxicosis with acute Wernicke encephalopathy: a case report. (2/33)
A 35-year-old hyperthyroid woman who developed nausea, vomiting, tachycardia, nystagmus and mental disturbance, was referred to our hospital with a suspected diagnosis of thyroid storm. However, the thyroid gland was only slightly palpable, bruits were not audible, and exophthalmos was not present. Serum levels of thyroid hormone were increased, but TSH receptor antibodies were negative. Echography and color flow doppler ultrasonography revealed a slightly enlarged thyroid gland and a slightly increased blood flow, both of which were much less milder than those expected for severe hyperthyroid Graves' disease. Under the diagnosis of hyperthyroidism due to gestational thyrotoxicosis associated with Wernicke encephalopathy, vitamin B1 was administered on the first day of admission. Her consciousness became nearly normal on the second day except for slight amnesia. Her right abducent nerve palsy rapidly improved, but horizontal and vertical nystagmus, diminished deep tendon reflexes and gait ataxia improved only gradually. MRI findings of the brain were compatible with acute Wernicke encephalopathy. We concluded that history taking and physical findings are important to make a differential diagnosis of gestational thyrotoxicosis with acute Wernicke encephalopathy from Graves' thyroid storm, and that Wernicke encephalopathy should be treated as soon as possible to improve the prognosis. (+info)A case of thyroid storm due to thyrotoxicosis factitia. (3/33)
We describe a case of thyroid storm due to thyrotoxicosis factitia, which was caused by the ingestion of excessive quantities of exogenous thyroid hormone for the purpose of reducing weight. An 18-year-old female was admitted to the hospital 24 hours after taking up to 50 tablets of synthyroid (1 tablet of synthyroid : levothyroxine 100 microg). Because of her stuporous mental state and acute respiratory failure, she was intubated and treated in the intensive care unit. After reviewing her history carefully and examining plasma thyroid hormone levels, we diagnosed this case as a thyroid storm due to thyrotoxicosis factitia. Her thyroid function test revealed that T3 was 305 ng/dL, T4 was 24.9 microg/dl, FT4 was 7.7 ng/dL, TSH was 0.05 micro IU/mL and TBG was 12.84 microg/mL (normal range: 11.3 - 28.9). TSH receptor antibody, antimicrosomal antibody, and antithyroglobulin antibody were negative. She was recovered by treatment, namely, steroid and propranolol, and was discharged 8 days after admission. Thyroid storm due to thyrotoxicosis factitia caused by the ingestion of excessive thyroid hormone is rarely reported worldwide. Therefore, we now report a case of thyroid storm that resulted from thyrotoxicosis factitia caused by the ingestion of a massive amount of thyroid hormone over a period of 6 months. (+info)Rhabdomyolysis accompanying thyroid crisis: an autopsy case report. (4/33)
Rhabdomyolysis is occasionally associated with metabolic disorders such as diabetic coma, severe electrolyte disturbances and myxedema coma. We describe rhabdomyolysis accompanying thyroid crisis. A 50-year-old man with Graves' disease developed rhabdomyolysis, congestive heart failure and hepatic failure during the course of thyroid crisis and then died of acute renal failure. Postmortem examination revealed rhabdomyolysis in the cardiac and psoas muscles, old myocardial infarction, hepatic centrilobular necrosis, renal cortical necrosis, and follicular hyperplasia in the thyroid. Circulatory collapse and dehydration under excessive hypermetabolic state presumably suppressed the source of energy and oxygen for muscle cells, leading to cellular damage. (+info)Thyroid storm associated with probable subclinical hypoadrenocorticism in an elderly woman. (5/33)
A 73-year-old woman was admitted to the hospital for severe persistent vomiting with fever, drowsiness, and weight loss. Elevated serum levels of thyroid hormones and the presence of a consciousness disorder with fever and vomiting led to the diagnosis of thyroid storm. A low normal concentration of serum cortisol, urinary 17-hydroxycorticosteroids and an elevated plasma level of corticotropin suggest that an inadequate adrenal reserve have been involved in the pathogenesis of the thyroid storm in this patient. She responded to the administration of intravenous methimazole and oral supersaturated potassium iodide solution. (+info)Decreases in alpha beta T cell receptor negative T cells and CD8 cells, and an increase in CD4+ CD8+ cells in active Hashimoto's disease and subacute thyroiditis. (6/33)
We examined peripheral lymphocyte subsets in patients with autoimmune thyroid disease, or subacute thyroiditis, in the active stage when possible. During destructive thyrotoxicosis arising from alpha beta T cell receptor (TCR) negative T (WT31-CD3+) cells and CD8 (CD4-CD8+) cells decreased and those of CD4+CD8+ cells increased slightly, resulting in proportional increases in CD4 (CD4+CD8-) cells, non-T, non-B (CD5-CD19-) cells, and the CD4/CD8 cell ratio. Changes were similar in active subacute thyroiditis. During stimulative thyrotoxicosis in active Graves' disease, the numbers of such T lymphocyte subsets were not changed, but only the number of CD5+ B (CD5+CD19+) cells increased markedly, resulting in proportional decreases in total T (CD3+) cells, alpha beta+ TCR T (WT31+CD3+) cells, CD8 cells, and non-T, non-B cells. A serial study of some of the patients showed opposite changes in alpha beta TCR- T cells, the CD4/CD8 cell ratio, and CD5+ B cells between the active stages of Graves' and Hashimoto's diseases. alpha beta TCR- T cells were mostly gamma delta TCR+ T (IIF2+ CD3+) cells in these patients. These data suggest that alpha beta TCR-T (gamma delta TCR+ T), CD8, and CD4+ CD8+ cells are important in thyroid destruction in Hashimoto's disease and subacute thyroiditis, and that CD5+ B cells are important in thyroid stimulation in Graves' disease. (+info)Juvenile thyrotoxicosis; can we do better? (7/33)
Thyrotoxicosis remains a frustrating condition for the young person, family, and health professionals involved. The associated symptoms do not always suggest thyroid disease and patients can be unwell for many months before the diagnosis is made. The antithyroid drug regimen used to treat children and adolescents with thyrotoxicosis varies from one unit to another and yet the potentially life threatening side effects and remission rates post-treatment may be related to the regimen used. Most patients with thyrotoxicosis will need many years of drug therapy if the thyroid gland is not removed surgically or destroyed by radioiodine. Even "definitive" treatment will typically necessitate thyroxine replacement for life. (+info)Severe starvation hypoglycemia and congestive heart failure induced by thyroid crisis, with accidentally induced severe liver dysfunction and disseminated intravascular coagulation. (8/33)
A 69-year-old woman caught a cold resulting in nausea, vomiting, diarrhea and severe anorexia. Then she suffered progressively from dyspnea and leg edema, and finally became delirious. On admission severe hypoglycemia, hypothermia, marked tachycardia, generalized edema, mild jaundice and cachexy were noted. EKG showed atrial fibrillation. A chest X-ray, chest CT and echocardiography showed congestive heart failure. Therapeutic use of diuretics induced shock leading to serious liver dysfunction and disseminated intravascular coagulation. However, combined therapy by intravenous glucose, digitalis, diuretics, anti-fibrinolytic drug and hydrocortisone were effective. Addition of antithyroid therapy brought a further favorable outcome. (+info)A thyroid crisis, also known as thyrotoxic crisis or storm, is a rare but life-threatening condition characterized by an exaggerated response to the excess production of thyroid hormones (thyrotoxicosis). This condition can lead to severe hypermetabolic state, multi-organ dysfunction, and cardiovascular collapse if not promptly diagnosed and treated.
Thyroid crisis is often triggered by a stressful event, infection, or surgery in individuals with uncontrolled or poorly managed hyperthyroidism, particularly those with Graves' disease. The symptoms of thyroid crisis include high fever, tachycardia (rapid heart rate), hypertension (high blood pressure), agitation, confusion, delirium, vomiting, diarrhea, and sometimes coma.
The diagnosis of thyroid crisis is based on the clinical presentation, laboratory tests, and imaging studies. Treatment typically involves hospitalization in an intensive care unit, administration of medications to block the production and release of thyroid hormones, control heart rate and rhythm, correct electrolyte imbalances, and provide supportive care until the patient's condition stabilizes.
Methimazole is an anti-thyroid medication that is primarily used to treat hyperthyroidism, a condition in which the thyroid gland produces excessive amounts of thyroid hormones. It works by inhibiting the enzyme thyroperoxidase, which is essential for the production of thyroid hormones. By blocking this enzyme, methimazole reduces the amount of thyroid hormones produced by the thyroid gland, helping to restore normal thyroid function.
Methimazole is available in oral tablet form and is typically taken two to three times a day. Common side effects of methimazole include nausea, vomiting, skin rashes, and joint pain. In rare cases, it can cause more serious side effects such as liver damage or agranulocytosis (a severe decrease in white blood cell count).
It is important to note that methimazole should only be used under the close supervision of a healthcare provider, as regular monitoring of thyroid function and potential side effects is necessary. Additionally, it may take several weeks or months of treatment with methimazole before thyroid function returns to normal.
Antithyroid agents are a class of medications that are used to treat hyperthyroidism, a condition in which the thyroid gland produces too much thyroid hormone. These medications work by inhibiting the production of thyroid hormones in the thyroid gland. There are several types of antithyroid agents available, including:
1. Propylthiouracil (PTU): This medication works by blocking the enzyme that is needed to produce thyroid hormones. It also reduces the conversion of thyroxine (T4) to triiodothyronine (T3), another thyroid hormone, in peripheral tissues.
2. Methimazole: This medication works similarly to propylthiouracil by blocking the enzyme that is needed to produce thyroid hormones. However, it does not affect the conversion of T4 to T3 in peripheral tissues.
3. Carbimazole: This medication is converted to methimazole in the body and works similarly to block the production of thyroid hormones.
Antithyroid agents are usually taken orally, and their effects on thyroid hormone production begin within a few hours after ingestion. However, it may take several weeks for patients to notice an improvement in their symptoms. These medications can have side effects, including rash, hives, and joint pain. In rare cases, they can cause liver damage or agranulocytosis, a condition in which the body does not produce enough white blood cells.
It is important to note that antithyroid agents do not cure hyperthyroidism; they only treat the symptoms by reducing thyroid hormone production. Therefore, patients may need to take these medications for several months or even years, depending on their individual circumstances. In some cases, surgery or radioactive iodine therapy may be recommended as alternative treatments for hyperthyroidism.
Hyperthyroidism is a medical condition characterized by an excessive production and release of thyroid hormones from the thyroid gland, leading to an increased metabolic rate in various body systems. The thyroid gland, located in the front of the neck, produces two main thyroid hormones: triiodothyronine (T3) and thyroxine (T4). These hormones play crucial roles in regulating many bodily functions, including heart rate, digestion, energy levels, and mood.
In hyperthyroidism, the elevated levels of T3 and T4 can cause a wide range of symptoms, such as rapid heartbeat, weight loss, heat intolerance, increased appetite, tremors, anxiety, and sleep disturbances. Some common causes of hyperthyroidism include Graves' disease, toxic adenoma, Plummer's disease (toxic multinodular goiter), and thyroiditis. Proper diagnosis and treatment are essential to manage the symptoms and prevent potential complications associated with this condition.
Propylthiouracil is a medication that is primarily used to treat hyperthyroidism, a condition characterized by an overactive thyroid gland that produces too much thyroid hormone. The medication works by inhibiting the production of thyroid hormones in the body. It belongs to a class of drugs called antithyroid agents or thionamides.
In medical terms, propylthiouracil is defined as an antithyroid medication used to manage hyperthyroidism due to Graves' disease or toxic adenoma. It acts by inhibiting the synthesis of thyroid hormones, triiodothyronine (T3) and thyroxine (T4), in the thyroid gland. Propylthiouracil also reduces the peripheral conversion of T4 to T3. The medication is available as a tablet for oral administration and is typically prescribed at a starting dose of 100-150 mg three times daily, with adjustments made based on the patient's response and thyroid function tests.
It's important to note that propylthiouracil should be used under the close supervision of a healthcare provider due to potential side effects and risks associated with its use. Regular monitoring of thyroid function tests is necessary during treatment, and patients should promptly report any signs or symptoms of adverse reactions to their healthcare provider.
The thyroid gland is a major endocrine gland located in the neck, anterior to the trachea and extends from the lower third of the Adams apple to the suprasternal notch. It has two lateral lobes, connected by an isthmus, and sometimes a pyramidal lobe. This gland plays a crucial role in the metabolism, growth, and development of the human body through the production of thyroid hormones (triiodothyronine/T3 and thyroxine/T4) and calcitonin. The thyroid hormones regulate body temperature, heart rate, and the production of protein, while calcitonin helps in controlling calcium levels in the blood. The function of the thyroid gland is controlled by the hypothalamus and pituitary gland through the thyroid-stimulating hormone (TSH).
An encyclopedia is a comprehensive reference work containing articles on various topics, usually arranged in alphabetical order. In the context of medicine, a medical encyclopedia is a collection of articles that provide information about a wide range of medical topics, including diseases and conditions, treatments, tests, procedures, and anatomy and physiology. Medical encyclopedias may be published in print or electronic formats and are often used as a starting point for researching medical topics. They can provide reliable and accurate information on medical subjects, making them useful resources for healthcare professionals, students, and patients alike. Some well-known examples of medical encyclopedias include the Merck Manual and the Stedman's Medical Dictionary.