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

In a retrospective study of 632 patients with pituitary disease we diagnosed pituitary insufficiency without hypersecretion of any pituitary hormone in 122 patients. Patients were substituted with sex hormones (76%), hydrocortisone (74%) and/or L-thyroxine (77%). 76% had additional growth hormone deficiency, as shown by an increase of growth hormone of less than 5 ng/ml after i.v. administration of L-arginine. In 17% of all patients the diagnosis of osteoporosis was proven or suspected radiologically. 57% had low bone mass of lumbar spine (dualphotonabsorptiometry) and 73% had low bone mass of the proximal forearm (singlephotonabsorptiometry). BMD values of pituitary insufficient patients were in the same range as those of patients with established osteoporosis. More than half of all patients (53%) complained of tiredness, exhaustion and muscle weakness. 40% suffered from adipositas. 77% had hyperlipidemia (68% hypertriglyceridemia and 42% hypercholesterinemia), 18% had hypertension. 14% of the patients had arteriosclerotic events in their history (myocardial infarction or stroke). These figures are higher than incidences shown in the German PROCAM-study. These data show an increased prevalence of osteoporosis and vascular diseases. This is in contrast to the general opinion, that patients with pituitary insufficiency are adequately treated by substitution with adrenal, thyroid and sex hormones. Whether other factors such as the additional growth hormone deficiency are responsible for these diseases has to be examined in prospective studies.
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PMID:[Increased prevalence of osteoporosis and arteriosclerosis in conventionally substituted anterior pituitary insufficiency: need for additional growth hormone substitution?]. 176 81

The manifestations of congenital rubella syndrome (CRS) can be grouped according to time of onset into newborn, extended, and delayed CRS. The delayed manifestations are not present in early life and include the following: endocrinopathies: diabetes, thyroid disease, and growth hormone deficiency; deafness; ocular damage: glaucoma, keratic precipitates, keratoconus, corneal hydrops, and absorption of the cataractous lens; vascular effects: fibromuscular proliferation of the intima, sclerosis of arteries, systemic hypertension secondary to renal disease, and subretinal neovascularization; and progressive rubella panencephalitis. Several mechanisms of pathogenesis of the damage have to be considered for the delayed manifestations, including growth of the virus in tissues, resulting in a reduced growth rate and shortened life-span of the cells; autoimmune responses, initially stimulated by the infection; genetic susceptibility; vascular damage by the viral infection with further stenosis or occlusion of the vessels later; reactive hypervascularization; and chronic persistence of the virus in the tissue with subsequent extension of the infection to other areas.
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PMID:Delayed manifestations of congenital rubella. 400 24

1. Growth hormone may influence cardiac growth during post-natal maturation or in response to hypertension, and the growth-hormone deficient dwarf rat model offers an opportunity to study this question. 2. We compared the blood pressure and heart weight of dwarf rats and Fischer (F344) control rats in early adulthood, after two hypertensive stimuli: unilateral renal ischaemia (two-kidney, one-clip) or the administration of deoxycorticosterone acetate and saline drinking fluid. 3. In untreated animals at 13 weeks of age the body weight of dwarf rats was significantly less than that of F344 rats, but the mean arterial pressure was similar. Although the hearts of dwarf rats were smaller than those of F344 rats, the heart weight/body weight ratio was significantly greater in dwarf rats. 4. Both dwarf and F344 rats developed similar hypertensive mean arterial pressures 5 weeks after left renal artery clipping or treatment with deoxycorticosterone acetate salt. The heart weights of hypertensive dwarf and F344 rats were equivalent, indicating a proportionally greater increase in cardiac size in dwarf rats for the same rise in blood pressure. 5. The plasma insulin-like growth factor-I level was markedly lower in dwarf than in F344 rats, and hypertension did not have any significant effects on these levels. 6. These findings indicate that the developmental increase in blood pressure and heart size in growing animals and the adaptive cardiac hypertrophy accompanying hypertension are not affected by growth hormone deficiency.
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PMID:Hypertension and cardiac hypertrophy in growth hormone-deficient rats. 792 70

Patients with adult onset growth hormone deficiency have a decreased life expectancy owing to an increased mortality from cardiovascular disease. In the present study, 104 subjects (66 men and 38 women, aged 22-74 years) with growth hormone deficiency and with adequate replacement therapy with glucocorticoids, thyroid hormones and gonadal steroids were studied with respect to known risk factors for cardiovascular disease. For comparison, data from a population study, "the MONICA study", were obtained. The patients had a significantly higher body mass index compared to controls (p < 0.001). Serum triglyceride concentration was higher (p < 0.001) but there was no difference in serum total cholesterol concentration. Serum high-density lipoprotein cholesterol concentration was lower (p < 0.001) in the patients. There was no difference in the prevalence of diabetes mellitus. The prevalence of treated hypertension was higher (p < 0.05) in the patients but the prevalence of smoking was lower (p < 0.001). Even after taking the increased body mass index into consideration, the changes in the prevalence of treated hypertension (p < 0.05) and in the serum concentrations of triglycerides (p < 0.05) and high-density lipoprotein concentrations (p < 0.001) remained. These results indicate that growth hormone deficiency alters lipoprotein metabolism and increases the risk for development of hypertension, which in turn might contribute to the increased risk for cardiovascular disease.
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PMID:Cardiovascular risk factors in adult patients with growth hormone deficiency. 821 83

Benign intracranial hypertension (BIH) is reported in three children from Australia and one from New Zealand, who were being treated with recombinant human growth hormone (rhGH). Three males and one female, aged between 10.5 and 14.2 y, developed intracranial hypertension within 2 weeks to 3 months of starting treatment. A national database, OZGROW, has been prospectively collecting data on all 3332 children treated with rhGH in Australia and New Zealand from January 1986 to 1996. The incidence of BIH in children treated with growth hormone (GH) is small, 1.2 per 1000 cases overall, but appears to be greater with biochemical GHD (<10 IU ml(-1)), i.e. 6.5/1000 (3 in 465 cases), relative risk 18.4, 95% confidence interval 1.9-176.1, than in all other children on the database. The incidence in patients with Turner's syndrome was 2.3/1000 (1 in 428 cases). No cases in patients with partial GHD (10-20 IU ml(-1)) or chronic renal failure were identified. Possible causative mechanisms are discussed. The authors' practice is now to start GH replacement at less than the usual recommended dose of 14 IU m(-2) week(-1) in those children considered to be at high risk of developing BIH. Ophthalmological evaluation is recommended for children before and during the first few months following commencement of rhGH therapy and is mandatory in the event of peripheral or facial oedema, persistent headaches, vomiting or visual symptoms. The absence of papilloedema does not exclude the diagnosis.
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PMID:Benign intracranial hypertension and recombinant growth hormone therapy in Australia and New Zealand. 962 91

Aortic stiffening is as much an important risk factor in cardiovascular morbidity and mortality, as it serves as reliable surrogate marker for clinical endpoints like myocardial and cerebrovascular incidents. Elevated aortic stiffness induces high systolic blood pressure, augmented pulse pressure with increased ventricular afterload, reduced subendocardial blood flow and augmented pulsatile stress in the peripheral arteries. Factors with relevant impact on the epidemiology of arterial stiffness are widely spread. 3 major groups of parameters influencing the stiffness of the aorta and the large arteries have been studied and described up to now: (i) physiological properties like age, gender, body height, pressure, hormonal state, genetic factors; (ii) environmental factors like nutrition (fish-, salt-, garlic consumption), smoking, performance of sports and aerobic capacity; (iii) diseases like hypertension, hypercholesterolemia, diabetes, coronary heart disease, cerebrovascular disease, renal failure, Marfan-syndrome, growth hormone deficiency. Close association between several of these factors impedes analyzing them independently from each other. Age and blood pressure were found to be the most prominent predictors of arterial stiffness in normal as well as in disease populations. Physiological and environmental factors can modulate these effects of aging, diseases generally seem to amplify them.
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PMID:Epidemiology of the arterial stiffness. 1047 71

The possible hormonal interactions of parathormone and extracellular calcium level with other endocrine systems were studied. Primary hyperparathyroidism was used first as a clinical model, in which hypercalcemia and normocalcemia occurs before and after surgery, respectively. An increased activity of renin-aldosterone system related to parathormone was found in hyperparathyroidism, and surgery resulted in a small decrease in blood pressure. This change was accompanied by a significant decrease in the activity of the renin-aldosterone system indicating the cessation of the secondary hyperaldosteronism. The role of a relative hyperinsulinism, occurring in hyperparathyroidism, in the pathogenesis of hypertension was not proved. The basal and stimulated secretion of thyreotrophin, the basal growth hormone level, and the stimulated prolactin secretion increased after surgery. Follicle stimulating hormone and luteinizing hormone secretions remained unchanged. The results suggest that extracellular calcium may reversibly modify the secretion of certain anterior pituitary hormones and their stimulus-induced responses. In the second disease, growth hormone deficiency syndrome, studied, long-term growth hormone replacement therapy results in significant but transient changes in bone metabolism: calcium-, alkaline phosphatase-, and phosphate levels increase until 6 to 18 months as compared to the initial values; then these parameters decrease to the baseline level. Parathormone decreases until the first year then returns to the baseline level. Osteocalcin shows similar temporary changes. In spite of the above transient changes, osteodensity increases after 12 months of treatment, and further improvement can be seen after 18 and 24 months, i.e. GH treatment exerts a biphasic effect on bones; resorption increases first followed by an increase in formation. Based on the above results, it can be concluded that both parathormone and extracellular calcium are able to influence the secretion of certain hormones; and--as it is shown in growth hormone replacement therapy--other hormones may cause certain effect on them, too. The better understanding of these interactions may result in a better understanding of the pathomechanism of certain diseases and the improvement of their treatment.
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PMID:[Hormonal interactions of parathormone and calcium metabolism]. 1263 47

IGF-I acts on vascular endothelium to activate nitric oxide synthase, thereby promoting vascular health; there is reason to believe that this protection is especially crucial to the cerebral vasculature, helping to ward off thrombotic strokes. IGF-I may also promote the structural integrity of cerebral arteries, thereby offering protection from hemorrhagic stroke. These considerations may help to explain why tallness is associated with low stroke risk, whereas growth hormone deficiency increases stroke risk--and why age-adjusted stroke mortality has been exceptionally high in rural Asians eating quasi-vegan diets, but has been declining steadily in Asia as diets have become progressively higher in animal products. There is good reason to suspect that low-fat vegan diets tend to down-regulate systemic IGF-I activity; this effect would be expected to increase stroke risk in vegans. Furthermore, epidemiology suggests that low serum cholesterol, and possibly also a low dietary intake of saturated fat--both characteristic of those adopting low-fat vegan diets--may also increase stroke risk. Vegans are thus well advised to adopt practical countermeasures to minimize stroke risk--the most definitive of which may be salt restriction. A high potassium intake, aerobic exercise training, whole grains, moderate alcohol consumption, low-dose aspirin, statin or policosanol therapy, green tea, and supplementation with fish oil, taurine, arginine, and B vitamins--as well as pharmacotherapy of hypertension if warranted--are other practical measures for lowering stroke risk. Although low-fat vegan diets may markedly reduce risk for coronary disease, diabetes, and many common types of cancer, an increased risk for stroke may represent an 'Achilles heel'. Nonetheless, vegans have the potential to achieve a truly exceptional 'healthspan' if they face this problem forthrightly by restricting salt intake and taking other practical measures that promote cerebrovascular health.
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PMID:IGF-I activity may be a key determinant of stroke risk--a cautionary lesson for vegans. 1294

It has been reported that adult patients with growth hormone deficiency (GHD) have increased risk factors for cardiovascular disorders in Western countries. However, data on this issue in Japan have not been fully investigated. To clarify the situation on this issue in Japan, a nationwide questionnaire survey was conducted by Study Group of Hypothalamo-Pituitary Disease, and medical records of 863 adult patients were recruited. The incidences of complications and risk factors for cardiovascular diseases were compared between GH deficient patients (GHD, n = 494) and GH intact patients (GHI, n = 369). The incidence of myocardial infarction was higher in GHD (1.2%) than in GHI (0.8%), but not significantly. The incidences of angina pectoris and liver dysfunction were significantly higher in GHD than in GHI (2.8 vs 0.8%, p = 0.048, and 11.9 vs 5.5%, p<0.0001, respectively). The prevalences of obesity and hyperlipidemia (HL) were significantly higher in GHD (p = 0.004, p<0.001, respectively). Combinations of HL plus diabetes mellitus (DM) or hypertension (HT) were more common in GHD than in GHI (HL + DM; 7.2 vs. 2.9%, HL + HT; 10.9 vs. 2.9%). These results indicated that GH deficiency have an increased prevalence of cardiovascular risk factors in Japanese similar to Western countries, and suggested that GH supplement therapy may be needed to reduce those complications.
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PMID:Complications in adults with growth hormone deficiency--a survey study in Japan. 1551 82

Clinical studies in patients with acromegaly have shown that growth hormone (GH) exerts both short- and long-term effects on the structure and function of the heart. Moreover, chronic growth hormone deficiency (GHD) has been associated with impaired cardiac performance, low heart rate and impaired left ventricular systolic function. Exercise capacity in patients with GHD is significantly reduced and in some severely affected individuals, dilated cardiomyopathy and heart failure has been reported. GHD has also been associated with a number of risk factors for cardiovascular disease. Altered lipoprotein metabolism and elevated fibrinogen and plasminogen activator inhibitor-1 activity are associated with GHD, and the risk of hypertension is increased in GH-deficient men. Subcutaneous and intra-abdominal fat mass have also been found to be abnormally high in these patients. These effects may contribute to an increased risk of death from cardiovascular disease. GH is therefore an important factor in the development and function of the cardiovascular system. In this paper, the effects of GH on the physiological mechanisms of the cardiovascular system are discussed, including the effect of GHD on cardiovascular disease risk. We will also discuss the effects of long-term GH replacement therapy in this patient population.
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PMID:Cardiovascular disease and risk factors: the role of growth hormone. 1559 64


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