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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 hormonal system is a communication system between cells and organs. Hence it is not surprising that it influences almost all physiological functions and, at least partially, our behaviour and fate. The sexual phenotype is determined by the sex hormones. Normally, the phenotype is in accordance with gonadal and genetic sex, but occasionally, as a consequence of enzymatic defects in the biosynthesis of sex hormones or of androgen resistance, gonadal and genetic sex are in discordance with the phenotype, the latter determining generally the civil sex and the sex of rearing. Whereas the gender role is generally determined by the sex of rearing and the phenotype, itself under hormonal influence, homo- and transsexuality constitute notorious exceptions to this rule. Although several authors consider homo- and transsexuality to be the consequence of an impairment in androgenic impregnation in the perinatal period, there are at present no convincing arguments for an hormonal origin for either homo- or transsexuality, although such a possibility can't be excluded either. Besides their role in psychosexual behaviour, sex hormones play also a role in our life expectancy. Indeed, although maximal life expectancy of man is genetically determined, a major determinant of individual life expectancy is cardiovascular pathology. The latter is partly responsible for the difference in life expectancy between men and women, cardiovascular mortality increasing rapidly at menopause and being halved by oestrogen replacement therapy. Also atherogenesis as such is, to a large extend, under hormonal control. Indeed insulin resistance and hyperinsulinism, which develop as a corollary of the aging process, is an important cause of atherosclerosis as well as of hypertension. Other hormones also play an important role in our behaviour. We can mention here the role of the thyroid hormones in the physical and mental development of children as well as in the regression of the intellectual functions in hypothyroidism; the role of growth (and sex) hormones in the clinical symptomatology of aging; the memory enhancing effects of the antidiuretic hormone; the role of growth factors (as well as of sex hormones) in tumorigenesis; the role of corticoids (and sex hormones) in the modulation of immunological processes etc. In brief, hormones influence all aspects of our life.
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PMID:[Do hormones determine our fate?]. 820 84

It has been demonstrated that high cholesterol levels are correlated with development of atherosclerosis, while high levels of high density lipoprotein (HDL) are associated with reduced cardiovascular mortality. Some endocrine disorders accelerate atherosclerosis in association with hypercholesterolemia, hypertension, low level of HDL and hypertriglyceridemia. In patients with acromegaly, hypertriglyceridemia is sometimes accompanied with and aggravated by the presence of impaired glucose tolerance. In patients with hypothyroidism, coronary atherosclerosis may develop in association with hypertension, hypercholesterolemia and moderate elevation of triglyceride which is often accumulation of intermediate lipoprotein. Cushing syndrome may accelerate atherosclerosis by the fact that corticosteroid may induce or exacerbate several known coronary risk factors including hypertension, hypercholesterolemia and impaired glucose tolerance. Estrogen has beneficial effects on the cardiovascular system for postmenopausal women by affecting lipid metabolism, decrease of LDL and increase of HDL.
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PMID:[Atherosclerosis and endocrine disorders]. 841 91

Physiologic changes in metabolism may make thyroid diseases difficult to diagnose during pregnancy. Such diagnoses depend principally on clinical acumen and an understanding of the alterations of laboratory values, particularly thyroid-stimulating hormone (TSH), induced by pregnancy. Untreated thyrotoxicosis may lead to abortion, stillbirth, neonatal death and low birth weight. The principal cause of thyrotoxicosis in pregnancy is Graves' disease, which may be treated with antithyroid drugs or surgery. The use of radioactive iodine is absolutely contraindicated during pregnancy. Hypothyroidism during pregnancy is associated with hypertension and premature labor. The goal of thyroxine replacement therapy is to maintain serum TSH levels in the normal range. Many thyroid conditions and treatments directly affect the fetus and the principal antithyroid drugs are secreted in breast milk. Both the mother and neonate require monitoring. In addition, autoimmune postpartum thyroiditis may recur following each pregnancy in susceptible patients.
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PMID:Thyroid disease during pregnancy. 854 48

Misdiagnosis of primary hypothyroidism may be due to its running under the mask of myocardiodystrophy, coronary heart disease, bacterial and allergic myocarditis, arterial hypertension. It may underlie edema or accompany malignancy (thyroid cancer, in particular). Accurate diagnosis is complicated by primary damage to one organ or system.
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PMID:[Therapeutic "masks" of primary hypothyroidism]. 864 32

Secondary hyperlipoproteinemias are found in connection with other primary organic diseases. Typical examples are those seen with diabetes mellitus, liver and kidney diseases. In addition there are changes induced by hormonal dysfunctions such as hypothyroidism, by the use of oral contraceptives or in postmenopausal women. During pregnancy there is a physiological transient increase in lipoproteins. In addition to primary organic diseases there are a number of exogenous factors such as obesity, malnutrition and alcohol abuse causing hyperlipidemia. The relation between hypertension and hyperlipidemia described as familial dyslipidemic hypertension is less well known. Obesity, hypertension, dyslipidemia, hyperuricemia and impaired glucose tolerance are the basic conditions of the metabolic syndrome. Familial combined hyperlipidemia is a genetically determined, dyslipidemic syndrome with a high prevalence among patients with coronary artery disease and stroke. As there are some links between familial combined hyperlipidemia and secondary hyperlipoproteinemias, this disease entity is discussed together in this paper. Familial combined hyperlipidemia is metabolically, genetically and by this on a molecular level closely linked to familial dyslipidemic hypertension as well as the metabolic syndrome. The exact mechanism of this disease is currently unknown.
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PMID:[Secondary disorders of lipid metabolism, metabolic syndrome and familial combined hyperlipidemia]. 865 Sep 33

Differential diagnosis of dementing diseases is very important to rule in the so-called treatable dementia. The new DSM-IV criteria for dementia include memory disturbances and one or more of aphasia, apraxia, or frontal lobe dysfunctions as essentials. Alzheimer disease requires, in addition, slowly progressive course and ruling out other brain or systemic diseases. Vascular dementia requires focal neurological or neuroimaging signs. Other diseases which cause dementia include chronic subdural hematoma, infection and brain tumor. CT or MRI can readily diagnose them if suspected and they may be treated. Systemic diseases associated with treatable dementia include electrolyte disturbances, hypothyroidism, vitamin deficiency, alcohol or drug intoxication, syphilis and HIV infection. Prevention of dementia seems to be the future problem as we could prevent cerebrovascular diseases by treating hypertension.
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PMID:[Clinical aspects of dementia]. 875 26

Cerebrovascular disease may be secondary to various disorders including hypothyroidism, sepsis, neoplasia, hypertension, vascular malformation, and coagulopathy. Brain infarction or hemorrhage should be suspected in an animal with a sudden onset of a focal brain lesion. The recent availability of CT and MRI has improved our ability to diagnose cerebrovascular disease in animals. Treatment is directed at maintaining adequate oxygenation of the brain, controlling elevations of ICP, treating seizures, and identifying and treating any underlying disease. With appropriate care, many animals can recover.
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PMID:Cerebrovascular disease. 881 57

Obstructive sleep apnea (OSA) is a disorder in which there is repetitive collapse and closing of the pharynx during sleep. There is growing evidence to suggest that this disorder is a major cause of essential hypertension (EH) and that successful treatment of OSA can reduce the blood pressure (BP) significantly. In addition many other patients with EH have milder forms of sleep related breathing disorders (SRBD) like snoring, and upper airway resistance syndrome (UARS) which, while not as severe as OSA, may be severe enough to also cause systemic hypertension. We therefore propose a unifying hypothesis-that many patients with EH may have sleep related breathing disturbances (SRBD) and treatment of these disorders may improve the BP. SRBD could also explain many of the epidemiological, clinical, hereditary, biochemical, hematological and physiological characteristics seen in EH. In addition, many types of secondary hypertension (those caused by excessive alcohol intake, chronic renal failure, diabetes, hypothyroidism or acromegaly) have a higher than normal prevalence of OSA and OSA may contribute to the hypertension and organ damage found in these conditions as well. Thus SRBD may play an important role in the production of many cases of essential and secondary hypertension, and their early detection and treatment could reduce the hypertension and organ damage seen in these conditions.
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PMID:Essential and secondary hypertension and sleep-disordered breathing: a unifying hypothesis. 887 97

In the present study we evaluated the effects of methimazole, an antithyroid drug, on blood pressure and other variables in the early and established phases of hypertension induced by the inhibition of nitric oxide synthesis with the oral administration of NG-nitro-L-arginine methyl ester (L-NAME), 75 mg/100 ml in the drinking water. Moreover, we also evaluated the acute pressor effect of L-NAME on systemic blood pressure in control and rats treated chronically with methimazole, administered via drinking water (30 mg/100 ml). Oral administration of methimazole maintained the blood pressure of L-NAME-treated rats at normal levels 25 days after induction of hypertension. However, after 25 days of methimazole treatment in rats made hypertensive with L-NAME (for 25 days), high blood pressure was similar in methimazole-treated and non-treated L-NAME rats, despite the fact that a hypothyroid state had been achieved in the methimazole-treated rats. Acute intravenous injection of L-NAME caused a similar increase in mean arterial pressure in control and methimazole-treated rats at the lowest dose; however, smaller pressor responses were observed with increasing doses in hypothyroid rats. These results clearly demonstrate that hypothyroidism induced by methimazole prevents, but does not reverse, L-NAME hypertension and reduces the acute pressor responsiveness to L-NAME administration.
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PMID:Effects of methimazole in the early and established phases of NG-nitro-L-arginine methyl ester hypertension. 892 35


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