Hyperthyroidism caused by excessive consumption of sausages.

Hyperthyroidism results from excessive production of thyroid hormones. This is usually caused by Graves disease, but exogenous thyroid hormones can lead to similar symptoms. Recognition of the latter is difficult as excessive intake of thyroid hormone is not usually admitted nor recognised. To our knowledge, exogenous hyperthyroidism caused by thyroid-contaminated food has been described twice, but not in the Netherlands. A 77-year-old man presented at the Outpatient Department of Internal Medicine with lab values revealing hyperthyroidism. There were no abnormal findings at the physical examination. Antibodies against the thyroidstimulating hormone (TSH) receptor were not detectable. Thyroid scintigraphy with 123I showed an uptake of less than 1%. Silent thyroiditis was diagnosed and the natural course was awaited, but with no improvement in the thyroid values. The thyroglobulin was very low. Further anamnesis revealed an excessive daily consumption of sausages. Thyroid hormones were detectable in these sausages. After the patient stopped eating them, he became and remained euthyroid. The case stipulates the importance of a thorough anamnesis.

A case of thyroid storm due to thyrotoxicosis factitia.

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.

A Case of Thyroid Storm Due to Thyrotoxicosis Factitia

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 microgram). 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 microgram/dl, FT4 was 7.7 ng/dL, TSH was 0.05 micro IU/mL and TBG was 12.84 microgram/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.

The age of patients with thyrotoxicosis factitia in Italy from 1973 to 1996.

Thyrotoxicosis factitia, a syndrome due to the surreptitious ingestion of excess thyroid hormones, has generally been diagnosed in young or middle-aged women with psychopathological disturbances. We reviewed all the cases seen at our Institution over a 24-yr period, from 1973 to 1996. All 25 patients were women. Analysis was restricted to 17 patients who were born and lived in Tuscany (our region), since only these patients were distributed during the whole observation period. Diagnosis of thyrotoxicosis factitia was based on the following parameters: elevated serum total and/or free thyroid hormone levels, undetectable serum thyrotropin levels, low/undetectable serum thyroglobulin concentration, normal urinary iodine excretion, low/suppressed thyroidal radioactive iodine uptake (RAIU), absence of goiter, absence of circulating anti-thyroid antibodies. Surreptitious ingestion of thyroid hormone pill was eventually admitted by all patients. Age at diagnosis was >50 yr in 7/17 patients (41%): 6 of them were distributed in the period 1995-1996, and one in 1988. Patients older than 60 yr were 5/17 (29%), all in the last two years of the period under investigation. There was an increase in the age of patients with thyrotoxicosis factitia (p=0.02), which lost a statistical significance when the patients of the 1995-1996 period were excluded from analysis (p=0.88). This study provides evidence of an increased age of patients with thyrotoxicosis factitia in more recent years. From a practical standpoint, our study suggests that thyrotoxicosis factitia should be suspected and adequately looked for even in old patients with thyrotoxicosis of inexplicable origin, especially in the absence of goiter and thyroid autoimmune phenomena, and when common causes of low-RAIU hyperthyroidism, such as a load with iodine-containing drugs or subacute thyroiditis, have been excluded.

Color flow Doppler sonography in thyrotoxicosis factitia.

Color flow doppler sonography (CFDS) is a powerful technique which displays tissue blood flow and vascularity. Hyperthyroidism due to Graves' disease is characterized by variable degrees of increased blood flow at CFDS. The purpose of this study was to evaluate CFDS patterns in five women with thyrotoxicosis factitia, a condition due to surreptitious ingestion of excess thyroid hormone. Diagnosis was supported by the finding of elevated free thyroxine (FT4), ranging 24.2-67.6 pmol/L (normal values: 8.3-20.5), elevated free triiodothyronine (FT3), ranging 9.9-26.7 pmol/L (normal values: 3.8-8.4), undetectable thyrotropin (TSH), absent anti-thyroid antibodies, undetectable serum thyroglobulin (Tg) concentrations, very low/suppressed thyroidal radioiodine uptake and normal/low urinary iodine excretion. Moreover, all patients admitted thyroid hormone pills intake. All patients had normal thyroid volume and echogenicity at conventional sonography (mean estimated volume, 9.4 ml, range, 6-11 ml), and absent hypervascularity or minimal intrathyroidal vascular spots at CFDS. The peak systolic velocity (PSV) was at the lower limit of normal values (mean, 4 cm/sec, range 3-5 cm/sec). Twenty-six women with untreated Graves' disease had an increase in the mean PSV, (mean 12.9 cm/sec, range 8-20, p < 0.001) and diffuse hypervascularity. CFDS pattern in 24 normal women residing in the same area did not differ from that found in patients with thyrotoxicosis factitia. Thus, due to the nonthyroidal origin of excess thyroid hormone, CFDS showed absent hypervascularity and normal PSV in spite of a thyrotoxic status. These findings well correlate with the etiology of thyrotoxicosis factitia and may represent an additional, useful tool to confirm the diagnosis. For its easiness, rapidity (10 min) and noninvasive features, CFDS can be considered a first line test during office examination when thyrotoxicosis factitia is suspected.

Adverse effects of thyroid hormone preparations and antithyroid drugs.

Thyroid hormone preparations, especially thyroxine, are widely used either at replacement doses to correct hypothyroidism or at suppressive doses to abolish thyrotropin (thyroid-stimulating hormone) secretion in patients with differentiated thyroid carcinoma after total thyroidectomy or with diffuse/ nodular nontoxic goitre. In order to suppress thyrotropin secretion, it is necessary to administer slightly supraphysiological doses of thyroxine. Possible adverse effects of this therapy include cardiovascular changes (shortening of systolic time intervals, increased frequency of atrial premature beats and, possibly, left ventricular hypertrophy) and bone changes (reduced bone density and bone mass), but the risk of these adverse effects can be minimised by carefully monitoring serum free thyroxine and free liothyronine (triiodothyronine) measurements and adjusting the dosage accordingly. Thionamides [thiamazole (methimazole), carbimazole, propylthiouracil] are the most widely used antithyroid drugs. They are given for long periods of time and cause adverse effects in 3 to 5% of patients. In most cases, adverse effects are minor and transient (e.g. skin rash, itching, mild leucopenia). The most dangerous effect is agranulocytosis, which occurs in 0.1 to 0.5% of patients. This life-threatening condition can now be effectively treated by granulocyte colony-stimulating factor administration. Other major adverse effects (aplastic anaemia, thrombocytopenia, lupus erythematosus-like syndrome, vasculitis) are exceedingly rare.

Toxic emergencies of endocrine and metabolic therapeutic agents.

Treatment recommendations for insulin, sulfonylurea, and thyroid hormone poisoning are widely divergent. Recent research data indicates a standard approach to management of these poisonings. Clinical practice may now incorporate recent findings.

Clinical features and management of overdosage with thyroid drugs.

Accidental ingestion and overdose of medications used in thyroidal illnesses may occur because of the frequency of these diagnoses. This review discusses acute overdosage of 4 groups of medicines. Acute ingestion of thyroid replacement medications occurs very frequently. Overdosage in children is usually asymptomatic and a benign condition; after evacuation of the stomach, propranolol may be used to treat symptomatic children. Other therapeutic regimens are rarely indicated in this age group. Ingestions of large amounts of antithyroid medications occur very rarely and limited information regarding treatment is available in the medical literature. Acute ingestion of iodine often results in corrosive injury of the gastrointestinal tract and renal damage. Cardiopulmonary collapse secondary to circulatory failure, oedema of the epiglottis and aspiration pneumonias may cause death. Administration of starch and sodium thiosulphate, maintenance of airway and stabilisation of circulation are the major components of therapy. Acute overdosage of beta-blockers is uncommon but can be lethal. Patients may appear well initially but they can suddenly develop convulsions and profound cardiovascular collapse requiring instant aggressive therapy. Potassium and glucose concentrations should be monitored. The usage of atropine, isoprenaline (isoproterenol), glucagon and prenalteral is discussed.

[The possible role of disruptions of the cyclic AMP system in the pathogenesis of thyrotoxic myopathies]. / O vozmozhnoi roli narushenii sistemy tsAMF v patogeneze tireotoksicheskoi miopatii.

The value of kdiss of the "proteinkinase-cAMP" complex was increased 1.8-fold, number of the nucleotide binding sites was increased 3.7-fold with simultaneous decrease in cAMP concentration, when the cyclase system was studied in skeletal muscles of mice with experimental thyrotoxic myopathy. Activities of phosphodiesterase, adenylate cyclase, rate of activation of adenylate cyclase by adrenaline and sodium fluoride did not significantly differ as compared with normal values. Impairment of hormonal regulation of the cAMP-dependent processes is apparently responsible for multiple molecular and structural injuries in skeletal muscles in thyrotoxicosis.

[Drug-induced thyrotosic crisis or the dangers of an allegedly homeopathic preparation (author's transl)]. / Crise thyrotoxique médicamenteuse. Des dangers d'une préparation prétendue homéopathique.

Acute thyrotoxicosis following the ingestion of massive doses of thyroid hormone may pose diagnostic problems when the intoxication is clandestine, and may endanger life. The authors report here the case of a previously euthyroid young woman. The outcome was favourable, though assisted ventilation was required for a number of days. The particular features of this case (relatively low blood thyroxinelevels, anaemia and thrombocytopaenia following regression of the thyrotoxicosis, presence of parotid swelling) are discussed in the context of data from the literature.