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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Two of thousand pregnancies are complicated by a Graves' disease. The circumstances of diagnosis are usually maternal disorders (tachycardia, exophthalmia, loss of weight...), also fetal disorders (tachycardia, intra-uterine growth retardation, stillborn...). The discovery of fetal tachycardia (160 beats per minute), and maternal tachycardia (120 beats per minute) associated with high blood pressure, allowed us to suspect, in this case, a Graves' disease, responsible of fetal hyperthyroidism by autoantibodies crossing the placenta. The measuring of T3, T4, TSH and autoantibodies confirmed the diagnosis. The drug of choice is the PTU (propylthiouracil). It prevents synthesis of thyroid hormones and inhibits peripheral deiodination of T4 to T3. It treats simultaneously mother and fetus; the surveillance must allow us to adjust treatment to avoid fetal hypothyroidism, maternal thyrotoxicosis of peripartum and neonatal thyrotoxicosis.
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PMID:[Isolated fetal tachycardia, a diagnostic event of Basedow's disease. Apropos of a case]. 805 73

The results of hypothyreosis therapy with thyroideum (dried thyroid gland) were assessed in 40 patients. The study aimed at establishing proper dosage and assaying blood serum T4, T3, and TSH levels. Daily dose of 1 tablet (0.2 mg of iodine) improved clinical status but did not cover the daily requirement of the body for thyroid hormones. An increase in daily dose to 2 tablets (0.4 mg of iodine) produced nearly complete compensation of hypothyreosis. However, such a daily dose was often associated with adverse reactions, especially in patients with arterial hypertension or atherosclerosis. Thyroid hormones assay has shown that dried thyroid gland administered in daily dose of 0.4 mg normalizes serum T3 levels whereas serum T3 levels remained constantly low, and TSH increased as in non-treated disease. An increase of the daily dose to 0.6 mg of iodine produces excessive increase in serum T3 levels with clinical symptoms of T3 toxicity.
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PMID:[Outcome of treating hypothyroidism with thyreoideum]. 809 Jun 51

Previous reports of the follow-up of patients with atrial fibrillation have been confusing because of the variety of clinical presentations, heterogeneity of underlying pathology, and the initiation of follow-up at various stages of the patient's disease. The Canadian Registry of Atrial Fibrillation (CARAF) is a non-interventional, follow-up study of patients enrolled at the time of their initial diagnosis with atrial fibrillation at seven Canadian centres. At baseline, a comprehensive database recorded clinical, laboratory, and echocardiographic variables. No specific intervention was initiated and care was left to the attending physicians. Follow-up was performed at 3 months, 1 year, then annually. Echocardiograms were repeated every 2 years. Recurrence of atrial fibrillation, medical intervention, stroke, death, and other significant events have been specifically recorded. To date, 967 patients have been enrolled. Seven hundred and sixty-seven patients have been followed for 1 year, 468 for 2 years, and 217 for 3 years. Several studies have been undertaken on these patients. One study compared the variables of patients who were symptomatic with those who were asymptomatic. This study demonstrated that symptoms were more likely to occur if the patient were younger, had high blood pressure and high ventricular response during atrial fibrillation, and were female. These all achieve statistical significance and a formula was developed to predict the probability of symptoms in different subgroups of patients. Antiarrhythmic drug use was evaluated. Sotalol and propafenone were the most commonly used drugs and their use increased when atrial fibrillation was recurrent. Many patients initially received no antiarrhythmic drugs. Trends suggest that therapy is more aggressive with recurrence of the arrhythmia. The prevalence of thyroid abnormalities was investigated utilizing sensitive TSH measurements. This showed that overt hyperthyroidism is rare (1%) but laboratory abnormalities and history of thyroid dysfunction occurred more frequently, in 19% of patients. Another study evaluated antithrombotic therapy. Factors known to increase stroke risk, including congestive heart failure, previous stroke, and large left atrium all increased the use of anticoagulants. Anticoagulants were used more frequently in patients over the age of 65 and in patients with recurrent or chronic atrial fibrillation. There was concern that hypertension, shown to be a high predictor of stroke, did not result in a significant use of warfarin. Aspirin use was common in patients not placed on anticoagulants. Further studies are being undertaken with the ultimate goal to utilize baseline data to predict clinical outcomes.
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PMID:Follow-up of atrial fibrillation: The initial experience of the Canadian Registry of Atrial Fibrillation. 880 39

The aim of this study was to evaluate the relationship between subclinical hypothyroidism and/or autoimmune thyroid disease and coronary heart disease (CHD). Ninety seven patients diagnosed as having CHD by a coronary angiography (CHD group) and 103 healthy subjects matched for age, sex and body mass index (control group) were included in the study. Thyroid function, thyroid autoantibodies and serum lipid concentrations were measured in the CHD and control groups. The CHD group exhibited significantly decreased serum free T3 (FT3) and free T4 (FT4) levels, and significantly increased serum TSH levels as compared with the control group, indicating a significant decrease in thyroid function in the CHD patients. Serum high density lipoprotein cholesterol (HDL-C) levels were significantly decreased in the CHD group. The incidence of subclinical hypothyroidism and thyroid autoantibodies was similar in both two groups. These observations were also true of women even after those who had diabetes mellitus (DM), hypertension (HT) and a smoking habit were excluded. This was not the case, however, in men without DM, HT, or a smoking habit. Patients with CHD had significantly lower serum levels of HDL-C than the control subjects, regardless of gender (P < 0.01). In the group with CHD, there was no difference between the serum lipid levels in patients with subclinical hypothyroidism and those with normal thyroid function. Female patients with CHD had significantly lower serum levels of thyroid hormone and HDL-C, but their subclinical hypothyroidism or thyroid autoimmunity did not seem to be related to the development of CHD.
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PMID:Decrease in serum levels of thyroid hormone in patients with coronary heart disease. 907 5

Hypothyroidism during pregnancy occurs in 1/1600-2000 deliveries, according to the most recent publications. The most common causes are chronic autoimmune thyroid disease, radiodine-131 treatment, or surgical removal. The diagnosis is difficult to make on clinical grounds alone, even in advanced cases, and a high index of suspicion is needed. Some women are at high risk of developing hypothyroidism, and they should be screened. These women may have had previous treatment for hyperthyroidism; high-dose neck irradiation, evidence of thyroid autoimmunity, amiodarone therapy, suspected hypopituitarism, and type I diabetics. The best laboratory test is the serum TSH, followed, if elevated, by a free T4 index and a TPO-ab titer. Thyroid antibodies have been associated with an increased (double) risk of miscarriage and postpartum thyroiditis. Frequent (22-44%) pregnancy-induced hypertension leading to preterm delivery, and prematurity is the main complication observed in those still hypothyroid near term. Proper therapy eliminates or reduces the risk. No congenital anomalies have been reported in the most recent studies, and the data available shows that both physical and mental development have been normal until children are 10 years old. However, one study reported lower IQs in children of euthyroid women with positive TPO-ab than in children of TPO-ab negative mothers. Levothyroxine is the treatment of choice. Euthyroidism must be reached and maintained in a timely fashion. Many women need more thyroxine during pregnancy, and surveillance of thyroid function is needed throughout gestation to make dose adjustments when needed. During the postpartum periods the thyroxine requirements decrease to preconception levels.
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PMID:Management of hypothyroidism during pregnancy. 910 50

Biondi, Fazio, and colleagues recently reported that long term T4 treatment to suppress serum TSH markedly affects cardiac function. T4-treated patients had more symptoms [12.2 +/- 3.9 (+/-SD) vs. 4.2 +/- 2.3 by quantitative questionnaire], higher mean heart rate, increased incidence of atrial extrasystoles, increased interventricular septal thickness and left ventricular mass index (LVMi), and significant diastolic dysfunction. The severity of cardiac abnormalities was highly correlated with scores of a rating scale used for assessing symptoms of thyrotoxicosis. We have duplicated their studies in 17 athyreotic patients (mean age, 45 +/- 10 yr; range, 27-63 yr) without heart disease or hypertension whose dose of T4 was titrated to suppress serum TSH to less than 0.01 microU/mL. The mean duration of T4 treatment was 9.2 +/- 5.4 yr. Controls were healthy volunteers matched for sex and age (+/-3 yr). The mean T4 dose was 2.8 +/- 0.9 micrograms/kg (0.192 +/- 0.058 mg/day). By questionnaire, patients had minimal symptoms, although their symptom score was significantly greater than the control value (4 +/- 3 vs. 2 +/- 1; P < 0.05; maximum score, 36). No differences in mean heart rate or in atrial or ventricular extrasystoles were noted. In patients, indexes of systolic and diastolic function and interventricular septal thickness were similar to control values. The mean LVMi was normal in both groups. However, the mean LVMi in patients (117 +/- 35 g/m2) was higher than that in controls (92 +/- 31; P < 0.05). In conclusion, patients were minimally affected by TSH-suppressive doses of T4. They had few symptoms and no increase in extrasystoles or basal heart rate. Based on current knowledge, the increase in LVMi observed in patients without associated significant systolic or diastolic abnormalities does not have clinical or prognostic importance. Therefore, in the absence of symptoms of thyrotoxicosis, patients treated with TSH-suppressive doses of L-T4 may be followed clinically without specific cardiac laboratory studies.
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PMID:Minimal cardiac effects in asymptomatic athyreotic patients chronically treated with thyrotropin-suppressive doses of L-thyroxine. 966 56

Extrahypothalamic TRH participates in cardiovascular regulation and spontaneous hypertension of the rat. To investigate whether an increase in central TRH activity produces hypertension we studied the effect of the preTRH overproduction induced by I.C.V. transfection with a naked eukaryotic expression plasmid vector which encodes preTRH (pCMV-TRH). Northern blot analysis and RT-PCR showed that pCMV-TRH was transcribed in vitro and in vivo. At 24, 48, and 72 hours, pCMV-TRH (100 microg) in a significant and dose-dependent manner increased 37%, 84%, and 49%, respectively, the diencephalic TRH content and SABP (42+/-3, 50+/-2, and 22+/-2 mm Hg, respectively) with respect to the vector without the preTRH cDNA insert (V[TRH(-)]) as measured by RIA and the plethysmographic method, respectively, in awake animals. In addition, using immunohistochemistry we found that the increase of TRH was produced in circumventricular areas where the tripeptide is normally located. To further analyze the specificity of these effects we studied the actions of 23-mer sense (S), antisense (AS), and 3'self-stabilized sense (Ss) and antisense (ASs) phosphorothioate oligonucleotides against the initiation codon region. Only ASs inhibited the increase of TRH content and SABP induced by pCMV-TRH treatment. In addition, pCMV-TRH-induced hypertension seems not to be mediated by central Ang II or serum TSH. To summarize, central TRH overproduction in periventricular areas induced by I.C.V. transfection produces hypertension in rats which is reversed by specific antisense treatment. This model may help in testing effective antisense oligodeoxynucleotides against other candidate genes.
Hypertension 1997 Sep
PMID:Central overexpression of the TRH precursor gene induces hypertension in rats: antisense reversal. 932 19

Regulatory actions of angiotensin II (AngII), which is involved in the pathophysiology of hypertension and also participates in cell proliferation and cell differentiation, are mainly mediated by AngII type 1 (AT1) receptor. Recently, activating mutations of receptors causing hyperfunctioning endocrine diseases have been described in the case of the TSH and LH receptors, implicating that such mutations might occur in other G-protein-coupled receptors. Furthermore it seems to be possible that genetic variations of AT1 receptor have an influence upon the action of AngII. Therefore, we searched by sequence analysis of the coding region of AT1 receptor gene for activating mutations and genetic polymorphisms in 56 human adrenal tumors (16 aldosterone-producing adenomas, 10 cortisol-producing adenomas, 1 aldosterone-producing carcinoma, and 29 incidentalomas). We were not able to identify any activating mutation in the coding region of AT1 receptor gene. We conclude that activating mutations of the AT1 receptor are not a major cause of the development of adrenal adenomas, if at all. In addition, polymorphic subtypes of AT1 receptor do not seem to play a major role in the pathogenesis of these tumors, even though a tendency towards a higher frequency of the polymorphic base substitution at position 573 (T573-->C) in cortisol-producing tumors needs to be further evaluated.
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PMID:Absence of angiotensin II type 1 receptor gene mutations in human adrenal tumors. 933 May 90

We report a rare case of Cushing's syndrome due to bilateral adrenocortical adenomas in a 45-year-old female. She suffered from diabetes mellitus and hypertension for a decade, but her appearance was not Cushingoid. The plasma cortisol level in the morning was at the upper limit of the normal range, but did not show a diurnal rhythm or was suppressed by 1 mg of dexamethasone. The plasma level of ACTH was undetectable, and it failed to respond to human CRH (hCRH). Plasma cortisol responded well to synthetic ACTH. The urinary 17-OHCS level was high, and was not suppressed by 4 mg of dexamethasone. While these findings were consistent with a diagnosis of adrenocortical adenoma, computed tomography showed several nodules in both adrenal glands that suggested the presence of huge nodular adrenocortical hyperplasia or bilateral adrenocortical adenomas. Bilateral adrenalectomy demonstrated the presence of three adenomas, two in the right and one in the left adrenal. Analysis of the extract from each adenoma revealed that two of the three produced an excess amount of cortisol. Magnetic resonance imaging (MRI) of the brain suggested the presence of pituitary adenoma. Prior to adrenalectomy, TSH, GH or LH showed a low response to TRH, GHRH or LHRH, respectively. Since normal responses were restored after bilateral adrenalectomy, these abnormalities were attributed to hypercortisolemia.
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PMID:A rare case of Cushing's syndrome due to bilateral adrenocortical adenomas. 944 86

Perturbations in the sympathetic nervous system may be anticipated in adults with hypopituitarism and untreated GH deficiency, because the syndrome is associated with both peripheral and central factors known to modulate sympathetic traffic. The higher prevalence of hypertension and increased cardiovascular morbidity/mortality reported in GH-deficient patients may suggest increased activity of the sympathetic nervous system. We recorded muscle sympathetic nerve activity (MSNA) in 10 hypopituitary adults with adequate hormonal replacement therapy except GH and in 10 healthy controls matched for age, gender, and body mass index to test whether hormonal aberrations in hypopituitarism and untreated GH deficiency are associated with an increase in sympathetic nerve traffic. Blood samples for insulin-like growth factor I, free T4, and TSH were taken after an overnight fast, followed by an oral glucose tolerance test. Direct intraneural recordings of MSNA were performed with a tungsten microelectrode from the peroneal nerve. The hypopituitary subjects had markedly increased MSNA (54 +/- 4 bursts/min vs. 34 +/- 4 in controls; P < 0.002), which was not related to abdominal obesity or altered glucose metabolism. When assessed for the whole study group, MSNA was inversely correlated to serum insulin-like growth factor I (r = -0.59; P < 0.006) and TSH (r = -0.46; P < 0.04). MSNA was positively correlated to diastolic blood pressure (r = 0.80; P < 0.0005) in patients, but not in controls. The intense sympathetic discharge is suggested to be of central origin and may be an important underlying mechanism for the secondary hypertension and increased cardiovascular morbidity/mortality in this patient group.
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PMID:Intense sympathetic nerve activity in adults with hypopituitarism and untreated growth hormone deficiency. 962 13


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