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

We report the case of a woman who had premature menopause, adrenal insufficiency and hypothyroidism by peripheral gland lesion, all most probably due to an autoimmune disorder, and who subsequently developed primary pulmonary arterial hypertension. The causes of this hypertension are ill-defined, but an autoimmune origin has often been envisaged since primary pulmonary arterial hypertension is not unfrequently associated with connective tissue diseases. Its association with an autoimmune polyendocrinopathy has only been reported, to our knowledge, on four occasions; in all 4 cases the thyroid gland was involved, and a connective tissue disease was present in 3 of them. Our case, which includes adrenal insufficiency and premature menopause is, as far as we know, unique. The possible link between these various diseases is their autoimmune nature, in which case primary pulmonary arterial hypertension would belong to the category of organ-specific autoimmune diseases. Our case supports the hypothesis that a number of isolated primary pulmonary arterial hypertensions could be of autoimmune origin.
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PMID:[Polyendocrinopathy combined with primary pulmonary arterial hypertension]. 252 20

The mortality rate from ischaemic heart disease (I.H.D.) has increased in young women by about 50% in 12 years, and it is now possible to report the findings in 150 women who developed symptoms and signs of I.H.D. under the age of 45. Data obtained from 145 of these women form the basis of this report: 81 presented with myocardial infarction and 64 with angina. In the remaining five there was a definite nonatherosclerotic cause for the premature onset of I.H.D.Hypercholesterolaemia, hypertension, or excessive cigarette smoking each occurred in a large minority, and more than one of these major risk factors was present in most patients. Hypercholesterolaemia was the commonest factor. In women in whom lipoprotein typing was undertaken the type II pattern was more frequent than type IV. The prevalence of hypercholesterolaemia and hypertension was the same in those with myocardial infarction and in those with angina.Excessive cigarette smoking was more common in women with myocardial infarction than in those with angina. The latter did not differ in their cigarette smoking habits from the normal population.A premature menopause had occurred in 20% of these women, but there was no relation between the early onset of I.H.D. with age at menarche, parity, or the incidence of abortion. Oral contraceptives did not increase the risk of myocardial infarction unless one of the major risk factors was also present.Altogether 75% of patients with angina or myocardial infarction survived 12 years. Coexisting hypertension worsened the prognosis. The prognosis after myocardial infarction was similar in these women to that previously described for men under the age of 40.
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PMID:Ischaemic heart disease in young women. 442 52

Oocyte donation was applied initially to women with hypergonadotrophic hypogonadism or 'premature menopause'. Later, therapy was extended to recipients > 40 years old and to post-menopausal women. In all cases, enhanced implantation and pregnancy rates were obtained by many investigators. Post-menopausal women must be informed about in-vitro fertilization results, obstetric risks for themselves and their newborn babies. They must be screened and investigated as accurately as possible for any existing medical contraindication. Results are encouraging because these patients become pregnant as easily as young donors, with pregnancy rates of 58, 34.6 and 37.9% per patient, per synchronization cycle and per transfer respectively. Abortion rates (5%) are very low considering the women are > 45 years old. The post-menopausal uterus can sustain implantation, grow and carry pregnancy to term and reduce adequately after labour. The incidence of maternal morbidity during pregnancy is less encouraging. A higher incidence of pregnancy-related diseases, e.g. gestational diabetes, hypertension, moderate and severe pre-eclampsia have been reported.
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PMID:Counselling post-menopausal women for donor in-vitro fertilization and hormone replacement therapy. 765 73

Elevated total blood cholesterol levels (at or above 240 mg/dL) due to increased low density lipoprotein (LDL) cholesterol values (at or above 160 mg/dL) have been associated with an increased risk of coronary heart disease (CHD). It has been shown in controlled prospective studies that when LDL cholesterol is lowered with diet or diet and drug treatment, subsequent risk of CHD morbidity and, in some cases, mortality can be reduced. New guidelines have recently been released by the Adult Treatment Panel (ATP II) of the National Cholesterol Education Program (NCEP). Risk factors for CHD in addition to elevated LDL cholesterol now include: 1) male 45 years or older; 2) female 55 or older, or with premature menopause and not on estrogen replacement; 3) high density lipoprotein (HDL) cholesterol less than 35 mg/dL; 4) hypertension; 5) cigarette smoking; 6) diabetes mellitus; and 7) a family history of premature CHD. After screening with total cholesterol and HDL cholesterol measurements, patients with total cholesterol values at or above 200 mg/dL, HDL cholesterol below 35 mg/dL, and/or CHD should have a fasting cholesterol, triglyceride, and HDL cholesterol measurement. Candidates for diet therapy are those with LDL cholesterol values at or above 1) 160 mg/dL; 2) 130 mg/dL in the presence of two or more CHD risk factors; or 3) 100 mg/dL in the presence of CHD. Candidates for drug therapy after diet treatment are those with LDL cholesterol values at or above 1) 190 mg/dL; 2) 160 mg/dL in the presence of two or more CHD risk factors; or 3) 130 mg/dL in the presence of CHD.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:New recommendations for the diagnosis and treatment of plasma lipid abnormalities. 830 97

Combining the wealth of epidemiological, metabolic and recent mechanistic data, it would appear biologically plausible that HRT, either oestrogen alone or in combination with progestogen, is cardioprotective. Further research is required, as information is lacking on cardiovascular effects of HRT instigated at an older age. There is a need to identify cardiovascular benefit, indirect and/or direct, of combined oestrogen/progestogen therapy using randomized trials. The various progestogen types and doses also need to be investigated. Studies are also required to investigate the effect of HRT use in higher risk patients with established CVD. There is scant information on the effect of HRT on blood pressure of patients with hypertension. Cardiovascular risk factor profiles and incidence surveys need to be conducted in developing countries to characterize their female population and to identify the prevalence of CVD; this needs to be undertaken before widespread recommendations on CVD prevention and the role of HRT can be made. If HRT is to be used effectively in the future treatment of heart disease in women these questions need to be addressed. At present HRT is indicated for the relief of menopausal symptoms and the prevention of osteoporosis. In women without these indications, ORT may be recommended in those who have had a premature menopause, and possibly in those who have established CHD or who are at high risk of developing CHD. It is too early to suggest a blanket recommendation for the use of HRT in the treatment of the symptoms of women with established CVD, but HRT after the menopause may at least be safely used in the secondary prevention of CHD.
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PMID:The menopause and the cardiovascular system. 893 7

The course of myocardial infarction (MI) in women, especially 60 years of age and older, is characterized by such severe complications as cardiorrhexis, hypovolemic cardiogenic shock, asystole, recurrent ventricular fibrillation and electromechanic dissociation responsible for the majority of lethal outcomes. Especially high MI lethality is in women at the age 70-79 years who have also the highest incidence of recurrent macrofocal MI while small-focal MI occurs in women over 80 years of age (80-89) more frequently than in 60-year-olds and younger. Dominating MI risk factors in women were the following: arterial hypertension detected in 81% patients under 60 and 90.8% cases over 60 years; abnormal lipid spectrum of blood including hypercholesterolemia (HCE), hypertriglyceridemia (HTE) and low concentration of HDLP cholesterol. HCE and HTE closely correlated with abdominal obesity irrespectively of age. Early menopause in women under 60 and diabetes mellitus of type 2 in older women, accumulation of two and more factors of risk contribute to development of coronary heart disease and MI, in females.
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PMID:[Myocardial infarction in women: risk factors and clinical features]. 1287 87

The Systemic Lupus International Collaborating Clinics/American College of Rheumatology (ACR) Damage Index (SDI) is an accepted instrument to ascertain damage. It has been shown to vary among different SLE populations. The aim of this study was to assess SDI score, pattern and factors related to damage in Brazilian SLE outpatients. The SDI was obtained in 105 patients with a median age of 41 (5-95%, 19-61.7) years and a median SLE duration of 127 (17.6-345.9) months. Patients had a median SDI of 2 (0-8) and 81.9% had some damage (SDI > 0). Damage was associated with a higher number of ACR criteria for SLE in multivariate analysis (OR = 2.32, 95%CI = 1.23-4.37, P = 0.009). Antiphospholipid syndrome (APS) (OR = 9.82, 95%CI = 2.74-35.23, P < 0.001), methylprednisolone pulses (OR = 3.91, 95%CI = 1.19-12.81, P = 0.024), age (OR = 1.70, 95%CI = 1.02-1.13, P = 0.011) and prednisone use duration (OR = 1.01, 95%CI = 1.002-1.02, P = 0.020) were related to severe damage (SDI > or = 4). Hypertension was associated with renal, cardiac and atherosclerotic damage, as cyclophosphamide pulses were with premature menopause. In conclusion, damage was very frequent in Brazilian SLE patients, mainly due to skin involvement, compared to other SLE populations. The presence of APS was the major independent contributor to the development of severe damage. Arterial hypertension was identified as a common risk factor for renal, cardiac and atherosclerotic damage.
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PMID:Rate, pattern and factors related to damage in Brazilian systemic lupus erythematosus patients. 1459 30

Turner syndrome is a condition usually associated with reduced final height, gonadal dysgenesis, and thus insufficient circulating levels of female sex steroids, and infertility. A number of other signs and symptoms are seen more frequently with the syndrome. With respect to cardiac function, congenital malformations of the heart and the great vessels, hypertension and ischemic heart disease, and increased risk of aortic dissection are all conditions that the pediatrician or the physician caring for females with Turner syndrome should keep in mind. Many girls and adolescents with Turner syndrome receive growth hormone (GH) treatment, which has so far been an effective and well-tolerated therapy. Nevertheless, because of the experience from acromegaly, the physician should monitor blood pressure and perform echocardiography, together with clinical examinations by a cardiologist at regular intervals. During adulthood most women with Turner syndrome are faced with premature menopause and the need for female hormone replacement therapy (HRT). During clinical evaluation of girls and women with Turner syndrome, these conditions and complications should be kept under surveillance. Here the cardiovascular complications of Turner syndrome are reviewed. The risk of congenital heart defects such as bicuspid aortic valves, aortic coarctation, other valve abnormalities, and septal defect is increased. Likewise, the risk of aortic dissection at a young age is increased, as is the risk of hypertension, ischemic heart disease, and stroke. GH therapy does not seem to adversely affect the heart, although longer-term follow-up studies are needed. In short-term studies, HRT lowers blood pressure, while any effect on the risk of ischemic heart disease has not been evaluated. Treatment with GH and HRT are discussed in relation to the heart and great vessels. Presently, the pathophysiology of the congenital cardiovascular malformation in Turner syndrome is unexplained, although different theories exist. Recommendations for clinical practice are given, including life-long surveillance of cardiac function, aortic diameter and blood pressure.
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PMID:Turner syndrome and the heart: cardiovascular complications and treatment strategies. 1472 55

Premature coronary heart disease (CHD) has emerged as a major cause of morbidity and mortality in patients with systemic lupus erythematosus (SLE). Overall SLE patients have a 5-6-fold increased risk of CHD and this excess risk is especially pronounced in younger women where the excess risk may be >50-fold. Studies from our group and others have also demonstrated that SLE patients have a higher prevalence of subclinical atherosclerosis compared with controls, with approximately 30% having evidence of subclinical involvement. It is important to consider what factors may underlie this excess risk. We have found that certain 'classic' risk factors, i.e. hypertension and diabetes mellitus, are more prevalent in SLE and that persistent hypercholesterolaemia independently predicts patients who will develop CHD. These risk factors alone do not completely explain the excess risk observed, and after adjusting for classic risk factors SLE remains independently associated with both clinical and subclinical outcomes. Certain other metabolic changes also occur more frequently in SLE, namely premature menopause, renal impairment, high triglycerides and higher plasma homocysteine. In addition, insulin resistance is more pronounced in patients with SLE, and approximately 18% have the metabolic syndrome. It is also increasingly accepted that atherosclerosis is a chronic inflammatory condition, and in SLE systemic complement activation as well as immune complex formation can result in changes that promote the development of atheroma. Similarly, autoantibody production, especially antibodies directed against lipoprotein subtypes and those in the antiphospholipid (APLA) family, are gaining increasing attention. The role of the latter are particularly controversial as different subtypes have been shown to both promote and protect against atherogenesis. In a study looking at carotid plaque in SLE, we found that APLA was independently associated with the presence of plaque; this study also found that patients with plaque had higher white cell counts, suggesting ongoing chronic inflammation. We have also noted a negative correlation between activation of transforming growth factor beta-1 and carotid intima-medial thickness. This cytokine, which is known to be a potent anti-inflammatory molecule, has also been shown to be protective against atherogenesis. With regard to therapy, steroids may be a true double-edged sword, with low doses exerting a beneficial anti-inflammatory role whereas higher doses may be detrimental through exacerbation of metabolic risk factors. In contrast, we have found that antimalarials have a beneficial effect on lipids especially when co-prescribed with steroids, and this, along with anti-inflammatory and proposed antiplatelet effects, may confer protection against CHD in lupus. The risk of premature CHD in SLE is therefore mediated by a number of factors that involve not only classic risk factors but also a range of factors associated with SLE itself. Preventative strategies will therefore need to address all potential risk factors of relevance. A more through understanding of the interplay between autoimmunity and atherogenesis should be possible by the study of SLE, and this may not only benefit lupus patients but also may have implications for our understanding of atherosclerosis in general.
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PMID:'Not only...but also': factors that contribute to accelerated atherosclerosis and premature coronary heart disease in systemic lupus erythematosus. 1623 77

Epilepsy in women is relatively often linked with reproductive disorders which include polycystic ovarian syndrome, hypothalamic amenorrhea and functional hyperprolactinaemia. These disorders have a significant share in a high incidence of infertility and premature menopause while the polycystic ovarian syndrome, also manifested by the metabolic syndrome, places the affected patients at risk of later consequences such as type 2 diabetes mellitus, cardiovascular diseases including arterial hypertension, gynaecological neoplasias (the breast and the endometrium), and in the case of pregnancy, a higher incidence of pregnancy induced hypertension. Apart from epilepsy as such, also antiepileptic treatment may have negative impact on the female's reproductive functions. In many cases, adverse effects of treatment complicate the patient's life more than the attacks alone. Medication induced weight gain might be responsible for different endocrine diseases (menstruation disorders, polycystic ovarian syndrome, hyperandrogenism). The article analyses the influence of side effects of the different antiepileptic drugs on the development of metabolic and endocrine anomalies. The role of antiepileptic drugs in the development of reproductive and endocrine disorders was first described by Isojarvim in 1993. A high incidence of polycystic ovarian syndrome and/or hyperandrogenism (43%) was observed in women taking valproat, which was clearly higher than in women taking other antiepileptics. Results reported in literature are rather controversial. The article gives an overview of current knowledge with respect to the influence of epilepsy and antiepileptics on the incidence ofpolycystic ovarian syndrome, which is considerably higher in women with epilepsy (10-25%) than in the unaffected population (4-7%), and of the related metabolic syndrome. The article concludes with recommendations for clinical practice in the treatment of epilepsy in women in reproductive age.
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PMID:[Epilepsy and disorders of reproduction]. 1747 15


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