[Fatal coronary artery spasm in a patient with thyrotoxicosis].

According to some data up to 20% of patients with thyrotoxicosis suffer from vasospastic angina. But presence of coronary artery spasm can be rarely confirmed. We describe a case of development of spasm of coronary arteries in a patients with severe thyrotoxicosis. Despite active treatment of thyrotoxicosis and use of drugs aimed at prevention of coronary spasm this patient with minor changes in coronary arteries (according to autopsy data) developed episode of acute myocardial ischemia leading to lethal outcome. This clinical case shows that patients with thyrotoxicosis and documented transitory myocardial ischemia should receive therapy with thyrostatics and drugs preventing coronary spasm in maximal doses until stable normalization of levels of thyroid hormones.

[Disturbances of thyroid function after coronary angiography].

Frequency of thyroid gland functional disturbances after introduction of iodine-containing radiographic contrast agents during coronary angiography was studied in 146 patients, residents of the zone of borderline iodine deficit. Frequency of thyroid pathology was high at baseline (39%). Functional state of the thyroid gland was assessed before and 1, 3, 6, 12 months after investigation. During first month after coronary angiography there were several new cases of thyrotoxicosis and hypothyroidism, as well as deterioration of preexisting functional disturbances of the thyroid. Patients with baseline pathology and functional disturbances of thyroid gland before conduction of coronary angiography should be included into risk group of development of iodine induced states.

[Diagnostics, treatment, and prevention of iatrogenic iodine-induced thyroid gland diseases].

The authors of the study investigated the effects of pharmacological doses of iodine as an ingredient of amiodaron, an anti-arrhythmic agent, and iodine radiopaque contrast agents (RCA), on the thyroid gland (TG) function. The subjects were 133 patients aged 60.5 +/- 8.5 years, who had been taking amiodaron for 12 to 164 months, and 164 patients aged 59.4 +/- 9.1 years, who were examined before coronarography (CAG) with RCA, and 1, 3, 6, and 12 months after the procedure. Serum levels of TSH, FT4, FT3, TG antibodies, TPO antibodies, and urine iodine level were measured; TG ultrasonography was performed. Forty-nine (51.9%) out of the 133 patients on amiodaron therapy developed thyroid disfunction. Subclinical hypothyroidism (24 cases; 18%) and manifest thyrotoxicosis (21 case; 15.8%) prevailed among functional TG disorders. Thirty-one per cent of the patients with thyrotoxicosis had preceding TG diseases; 70% of the thyrotoxicosis patients had a cardiac arrhythmia relapse. The concentration of thyroid antibodies did not change in patients with normal TG. The patients who underwent CAG displayed elevated renal iodine excretion 1, 3, and 6 months after RCA administration. Thyroid disfunction (thyrotoxicosis in 7.6% of the cases; hypothyroidism in 15.8% of cases) was revealed in 23.4% of the patients with preceding TG diseases one month after CAG. Cardial pathology exacerbation was observed in patients with thyrotoxicosis.

[Incidence and predictors of thyroid dysfunction caused by long-term intake of amiodaron].

AIM: To analyze occurrence of thyroid dysfunction due to regular long-term intake of amiodaron (for one year), to search for predictors of amiodaron-induced hypothyroidism and thyrotoxicosis. MATERIAL AND METHODS: Sixty two patients with different types of arrhythmia have undergone examination including tests for TTH (once in three months), free T3 and T4 (once in 6 months), ultrasound thyroid investigation, general clinical and physical check-up, resting ECG in 12 leads, echocardiography, chest x-ray, biochemical blood tests, blood count, urinalysis. RESULTS: Amiodaron intake for 1 year was associated with amiodaron-induced thyroid dysfunction in 25% patients: 19.2% developed hypothyroidism, 5.8%--thyrotoxicosis. Organic pathology of cardiovascular system, cardiac failure, left ventricular aneurysms, low global myocardial contractility, organic thyroid pathology, elevated levels of antithyroid antibodies predicted hypothyroidism. Thyrotoxicosis was associated with a young age and male sex. CONCLUSION: Amiodaron may cause thyroid dysfunction in patients with arrhythmia.

[Lipid blood spectrum in patients with amiodarone associated hypothyroidism. Effect of replacement therapy with L-thyroxine].

Blood lipid levels were measured in 23 patients with amiodarone associated hypothyroidism (most of them had ischemic heart disease). Abnormalities of lipid spectrum were found in 12 of these patients. All 12 patients were subjected to replacement therapy with l-thyroxine. Compensation of thyroid status was associated with average 12.6 and 12.3% lowering of total and low density lipoprotein cholesterol, respectively. However target levels of low density lipoprotein cholesterol were achieved only in 1 patient. There were no significant changes of high density lipoprotein cholesterol and triglycerides.

[Thyroid dysfunction in long-term amiodarone administration. Correlation of the antiarrhythmic activity of amiodarone with its effect on thyroid function].

Relationship between amiodarone-associated thyroid dysfunction and antiarrhythmic activity of amiodarone was studied in 27 patients (13 with hypothyroidism, 8 with hyperthyroidism, 6 with euthyroid hyperthyroxinemia). Amiodarone-associated hypothyroidism and euthyroid hyperthyroxinemia were not associated with loss of antiarrhythmic efficacy of amiodarone. Hypothyroidism did not require amiodarone withdrawal and therapy with L-thyroxin was conducted at the background of continued amiodarone intake. Achievement of euthyroid state was not followed by recurrence of heart rhythm disturbances. Development of amiodarone-associated thyrotoxicosis was accompanied with loss of antiarrhythmic efficacy of amiodarone in all cases. In 87.5% of patients with thyrotoxicosis correction of the thyroid status was conducted under conditions of continued amiodarone intake as this drug had been given because of life threatening arrhythmias or proven resistance to other antiarrhythmic therapy. In 12.5% of patients it was possible to substitute other drugs for amiodarone. Correction of thyroid status and achievement of euthyroidosis in these patients was associated with restoration of amiodarone antiarrhythmic activity.

[Amiodarone-associated thyroid dysfunction: prevalence and possibilities of correction]. / Amiodaron-assotsiirovannaia disfunktsiia shchitovidnoi zhelezy: chastota razvitiia, vozmozhnosti korrektsii.

During 1 year of amiodarone intake development of amiodarone-associated thyroid dysfunction was observed in 25% of patients (hypothyroidism and thyrotoxicosis in 19.2 and 5.8%, respectively). Development of hypothyroidism was not accompanied with loss of antiarrhythmic efficacy of amiodarone and therapy with L-thyroxin was conducted at the background of continued amiodarone intake. In all patients with clinical and in less than one half (47.6%) of patients with subclinical forms of hypothyroidism replacement therapy with L-thyroxin was carried out. Development of amiodarone-associated thyrotoxicosis was accompanied with loss of antiarrhythmic efficacy of amiodarone in all cases. In all patients with thyrotoxicosis which developed during amiodarone intake thyrostatic therapy with mercasolil was carried out and in case of its inefficacy prednisolone was added. In 87.5% of patients with thyrotoxicosis correction of the thyroid status was conducted under conditions of continued amiodarone intake as this drug had been prescribed because of life saving indications. Achievement of euthyroid state was followed by restoration of antiarrhythmic efficacy of amiodarone. Amiodarone was discontinued just in 1 patient with ventricular extrasystole as correction of thyroid status and restoration of euthyroidosis enabled effective use of other antiarrhythmic drugs.

[The specific features of thyrotoxicosis and euthyroid hyperthyroxinemia developed due to the use of cordarone]. / Osobennosti tireotoksikoza i eutireoidnoi gipertiroksinemii, razvivaiushchikhsia na fone priema kordarona.

Thyrotoxicosis (TT) is one of the thyroid (T) dysfunctions occurring with the use of cordarone. The clinical features of TT were studied in cordarone-treated patients living in Moscow and its regions (mild and moderate iodine deficiency regions). The patients were examined by using currently available procedures for measuring thyroid-stimulating hormone, free thyroxine, free triiodothyronine, antibodies to TH, TPO, interleukin-6 (IL-6), and C-reactive protein (CRP), and by employing T ultrasound study, Holter ECG monitoring. TT was ascertained to develop in the presence of both the pathologically altered (16/23, 69%) and intact T (7/23, 31%). Examining the course of cardiac arrhythmias (CA) in developed TT has established that this condition gives rise to their recurrence. As compared with the control group, the patients with TT were not found to have higher levels of IL-6 and CRP (p > 0.05; Mann-Whitney test). Therapy with thyrostatic agents alone or in combination with glucocorticosteroids normalizes the levels of thyroid hormonesfollowing, on the average, 2-3 months. Euthyroid hyperthyxinemia (EHT) is frequently recorded with the use of cordarone. Examination of 20 patients with EHT has revealed organic pathology in 13 (65%) patients and its absence in 7 (35%). Recurrences of prior CA have not been found in EHT (p < 0.05; McNemar test). The confidence interval for the difference of relative frequencies of signs did not include 0). Thus, TT is a condition that leads to the fact that cordarone loses its antiarrhythmic effects and TT requires compulsory treatment. If required, therapy should be performed during the continued administration of the drug. EHT is not thyrotoxicosis, which is to be followed up.

[Iodine deficiency in the Russian Federation]. / Ioddefitsitnye zabolevaniia v Rossiiskoi Federatsii.

Epidemiological surveys for iodine deficiency (ID) were made in 30 regions of Russia in 1992 to 1999. A total of 40,999 individuals aged 7 to 17 years were examined. The advent of new assessments of the thyroid and new indicators of iodine deficiency has changed approaches to epidemiological surveys. The WHO standards for estimating the prevalence and severity of ID have been introduced into Russian practice. In Central Russia, the lowest (median 30-58 micrograms/l) iodine concentrations were found in rural dwellers; in more urbanized areas (cities, towns) the median was 50-78 micrograms/l. ID was more pronounced in the regions of East Russia where it was predominantly moderate (median 30-52 micrograms/l). In some areas, ID was severe (median 16-20 micrograms/l). As the severity of ID increases, the incidence of such conditions, as goiter, hypothyroidism, endemic cretinism is on the rise. Mild to moderate goiter endemia prevailed in Central Russia. The manifestations of goiter endemia were more pronounced in rural children (18-30%) than in urban ones (8-14%). East Russia was marked by moderate to severe goiter endemia (8-14%): the incidence of goiter ranged from 17 to 40%. There were only sporadic cases of goiter in some areas of the Sakhalin Region. In the Moscow and Voronezh Regions and the Republic of Kalmykia there were areas showing a high goiter incidence which did not correspond to the level of ID. An epidemiological analysis has indicated that dietary and water iodine intake is decreased in most regions of Russia. The actual dietary iodine intake was 40-80 micrograms/day, i.e. 2-3 times of the recommended allowance (150 micrograms). The Endocrinology Research Center has tested different models of preventive and therapeutical measures for eliminating iodine deficiency-caused diseases by using iodinated foodstuffs (salt, bread, butter) ad iodine medicaments.

[Endemic goiter in Moscow and Moscow region]. / Sostoianie zobnoi éndemii v Moskve i Moskovskoi oblasti.

Goiter prevalence and iodine excretion levels were assessed in schoolchildren aged 9 and 13 in the city of Moscow (n = 91) and the Moscow region, 60 km East of Moscow (n = 92). Goiter prevalence was evaluated by ultrasonography. In Moscow it was found to be 31.1% among children aged 9 and 17.5% among those aged 13. The respective values in the Moscow region were 47.2 and 39.3%. Medium urinary iodine levels were 6.9 to 7.5 micrograms/dl in Moscow and 4.1 to 5.4 micrograms/dl in the region. According to modern criteria, iodine deficiency in Moscow may be regarded as mild and in the region as moderate. Control programs are urgently needed tc prevent development of iodine deficiency disorders.

[Determination of autoantibodies to thyrotropin receptors in patients with diffuse toxic goiter]. / Opredelenie autoantitel k retseptoram tireotropnogo gormona u bol'nykh diffuznym toksicheskim zobom.

The blood level of antithyroid autoantibodies to TSH receptors was determined in patients with toxic goiter (TG) before and during antithyroid therapy using two biological methods (by the increment in the cAMP level in slices and primary monolayer culture of human thyroid cells) and a radioreceptor method (by inhibition of TSH binding with its receptors from the animal thyroid). Comparison of the results of these three methods has shown that all methods are almost equally valuable for diagnosis of new cases of TG. However the biological method was shown to be more sensitive and informative with regard to predicting the time of immunological remission during antithyroid therapy.

[Morphofunctional features of the thyroid gland in patients with diffuse toxic goiter]. / Morfofunktsional'nye osobennosti shchitovidnoi zhelezy bol'nykh diffuznym toksicheskim zobom.

A study was made of the morphometric, ultrastructural and functional features of the thyroid in patients with diffuse toxic goiter (DTG) (women aged 16 to 12) with positive and negative dynamics of body mass (groups 1 and 2, respectively). Proliferation of the thyroid epithelium, detected in DTG patients of the 1st group, can be regarded as a morphological criterion for making a decision of a necessity of surgical intervention.

[Dynamics of thyrostimulating immunoglobulin levels during treatment of diffuse toxic goiter]. / Dinamika urovnia tireostimuliruiushchikh immunoglobulinov v protsesse lecheniia diffuznogo toksicheskogo zoba.

Twenty-five patients with diffuse toxic goiter, investigated at various time of mercazolyl therapy, demonstrated the presence of thyrostimulating immunoglobulins in 100% before treatment, in 91% after 6 months and in 50% after 12 months of treatment. Specific therapy reduced considerably not only the frequency of detection but also the activity of thyrostimulating immunoglobulins. Clinical and hormonal remission of disease did not always coincide with immunological remission.

[The carbohydrate metabolic characteristics of patients with diffuse toxic goiter proceeding with an increase in body weight]. / Osobennosti uglevodnogo obmena u bol'nykh diffuznym toksicheskim zobom, protekaiushchim s narastaniem massy tela.

Altogether 10 patients (aged 15 to 18) with Basedow's disease, accompanied by a growing body mass were investigated before operation and 5 patients 6 mos. after subtotal strumectomy. Ten patients with Basedow's diseases without body mass increment were taken as controls. A characteristic feature of carbohydrate metabolism in the study group as compared to the control group was hyperinsulinism with normal GTT which was preserved after doing away with thyrotoxicosis. The C-peptide/IRI ratio in patients with Basedow's disease, accompanied by a growing body mass, was decreased as compared to the control group, a tendency towards its increase after subtotal strumectomy was observed. Any differences in the levels of thyroid hormones, TSH and thyroid stimulating blood activity were undetectable.