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Accidental ingestion of poisons
... Although thyroid hormone intoxication is a not infrequent cause of poisoning in children, surprisingly few cases have been documented (Stanage and Henske, 1955). ...
Two girls aged 2 and 3 ingested a total of 1900 mg thyroid extract. The older girl had the higher serum T4 level and was treated by means of exchange transfusion.
During a period of four and a half years, eighty cases of accidental poisoning were admitted to the Medical College Hospital, Nagpur. The majority of these children were under the age of five years (62.5 per cent). Household poisons and poisonous plants accounted for the largest number of cases. Kerosene produced thirty-three cases (41.4 per cent) andchandrajyoti seeds seventeen cases (21.2 per cent). Three children died, all under the age of two. Preventive measures are suggested.
Thyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones. In most instances, thyrotoxicosis is due to hyperthyroidism, a term reserved for disorders characterized by overproduction of thyroid hormones by the thyroid gland. Nevertheless, thyrotoxicosis may also result from a variety of conditions other than thyroid hyperfunction. The present report focuses on the etiologies, pathophysiology and treatment of iatrogenic thyrotoxicosis. Iatrogenic thyrotoxicosis may be caused by 1) subacute thyroiditis (a result of lymphocytic infiltration, cellular injury, trauma or radiation) with release of preformed hormones into circulation, 2) excessive ingestion of thyroid hormones ("thyrotoxicosis factitia"), 3) iodine-induced hyperthyroidism (radiological contrast agents, topical antiseptics or other medications). Among these causes of iatrogenic thyrotoxicosis, that induced by the iodine overload and cytotoxicity associated with amiodarone represents a significant challenge. Successful management of amiodarone-induced thyrotoxicosis requires close cooperation between endocrinologists and endocrine surgeons. Surgical treatment may have a leading yet often underestimated role in view of the potential life-threatening severity of this disease, whereas others kinds of iatrogenic thyrotoxicosis are usually treated conservatively.
Serum thyreoglobulin (TG) levels continue to play a critical role in the diagnosis and management of a variety of thyroid disorders. In no situation is this more evident than in the management of patients afflicted with thyroid cancer. The ability to measure serum TG has not only significantly improved the management of these patients, but has also raised a number of new, clinically relevant questions. The intent of this article is to review the clinical utility of serum TG in a variety of thyroid disorders, with particular emphasis on the management of differentiated thyroid cancer. Assay limitations and potential solutions to these difficulties will be discussed
Thyrotoxicosis is a clinical syndrome caused by circulation of excess thyroid hormones. Classic hyperkinetic thyrotoxicosis is readily recognizable. Atypical presentations, however, can lead to diagnostic dilemmas. The sensitive thyroid-stimulating hormone assay has become an invaluable tool in the diagnosis of thyrotoxicosis. Causes of thyrotoxicosis include Graves' disease, toxic multinodular goiter, toxic adenoma, thyroiditis, inappropriate secretion of thyroid-stimulating hormone, trophoblastic tumor, exposure to iodine, and use of drugs. Increased uptake of radioidine by the thyroid gland differentiates true hyperthyroidism from other causes of thyrotoxicosis. Graves' disease is the most common cause of hyperthyroidism. It is caused by antibodies to the thyroid-stimulating hormone receptor that are stimulatory in nature. Extrathyroidal manifestations of Graves' disease include orbitopathy, dermopathy, and acropachy. Therapy includes thionamides, radioactive iodine, surgical intervention, and other adjunctive modalities. Thyroid storm is a medical emergency that necessitates prompt and aggressive therapy.
Thyrotoxicosis is the clinical syndrome that results when tissues are exposed to high levels of circulating thyroid hormones. In most instances thyrotoxicosis is due to hyperthyroidism, a term reserved for disorders characterized by overproduction of thyroid hormones by the thyroid gland. Nevertheless, thyrotoxicosis may also result from a variety of conditions other than thyroid hyperfunction. The present report focuses on the etiologies, pathophysiology, and treatment of iatrogenic thyrotoxicosis. Iatrogenic thyrotoxicosis may be caused by (1) subacute thyroiditis (a result of lymphocytic infiltration, cellular injury, trauma, irradiation) with release of preformed hormones into circulation; (2) excessive ingestion of thyroid hormones ("thyrotoxicosis factitia"); (3) iodine-induced hyperthyroidism (radiologic contrast agents, topical antiseptics, other medications). Among these causes of iatrogenic thyrotoxicosis, that induced by the iodine overload and cytotoxicity associated with amiodarone represents a significant challenge. Successful management of amiodarone-induced thyrotoxicosis requires close cooperation between endocrinologists and endocrine surgeons. Surgical treatment may have a leading yet often underestimated role in view of the potential life-threatening severity of this disease, whereas others kinds of iatrogenic thyrotoxicosis are usually treated conservatively.
Serum thyroglobulin measurement has greatly facilitated the clinical management of patients with differentiated thyroid cancer and a variety of other thyroid disorders. Thyroglobulin autoantibodies remain a significant obstacle to the clinical use of thyroglobulin measurement. The interpretation of any given thyroglobulin value requires the careful synthesis of all pertinent clinical and laboratory data available to the clinician. The diagnostic use of rhTSH-stimulated thyroglobulin levels has greatly facilitated the follow-up of low-risk patients with thyroid cancer. Although the measurement of thyroglobulin mRNA from peripheral blood is likely to affect the future management of these patients, it is expected that serum thyroglobulin measurement will continue to have a principal role in the care of patients with differentiated thyroid cancer.
ALTHOUGH desiccated thyroid is a widely dispensed medication, reports concerning its acute toxicity are sparse. Stanage and Henske,1 studying a series of 472 accidental poisonings in childhood, stated that thyroid was the third most common medication accidentally ingested, but they made no comment regarding any untoward effects that were observed. Jahr2 described 3 children, ranging in age from twenty months to three years, who accidentally took between 2.3 and 2.8 gm. of thyroid without marked side effects. Danowski and his co-workers3 have given large single doses of 1-thyroxine, equivalent to 0.128 gm. (or 2 gr.) of thyroid per kilogram of . . .
During a period of four and a half years, eighty cases of accidental poisoning were admitted to the Medical College Hospital, Nagpur. The majority of these children were under the age of five years (62·5 per cent). Household poisons and poisonous plants accounted for the largest number of cases. Kerosene produced thirty-three cases (41·4 per cent) andchandrajyoti seeds seventeen cases (21·2 per cent). Three children died, all under the age of two. Preventive measures are suggested.
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