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

However, side-effects such as severe infections, hypertension and electrolyte imbalance have been found, assumed to be related to hypercortisolism induced by chronic ACTH treatment. The authors treated 18 patients with infantile spasms with non-depot ACTH(1-24). The therapeutic effect of non-depot ACTH was comparable to that of depot ACTH, with no severe bacterial infection or sepsis. The incidence of hypertension was significantly lower in the non-depot ACTH group, and persistent hypercortisolaemia was not found. Non-depot ACTH(1-24) appears to be as effective as ACTH(1-24) depot therapy in the treatment of infantile spasms, and its side-effects are mild. It would appear that the effect of non-depot ACTH is not mediated by hypercortisolism, but by a direct neurotropic effect on the brain.
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PMID:The effect of non-depot ACTH(1-24) on infantile spasms. 825 87

A 46-year-old man with known arterial hypertension for 10 years had, over the last two years, developed increasing obesity, particularly of the trunk, with other symptoms typical of Cushing's syndrome. Hormone analysis demonstrated hypercortisolism and decreased plasma ACTH concentration. The dexamethasone inhibition test failed to show any significant suppression of serum cortisol. Plasma ACTH was not increased in the corticotrophin-releasing hormone and the metyrapone tests. In the short ACTH test there was an excessive cortisol increase. Abdominal computed tomography revealed both adrenals to be enlarged (6 x 4 cm) and coarsely nodular. Adrenolytic treatment with ketoconazole (400 mg daily) caused symptoms of adrenal insufficiency, but a reduced dosage of 200 mg daily lowered the cortisol level to between 5 and 11 micrograms/dl and normalized the blood pressure and clinical signs of Cushing's syndrome disappeared. Subsequent bilateral adrenalectomy confirmed the diagnosis of massive macronodular adrenal hyperplasia. Substitution treatment with twice daily 25 mg cortisone acetate and 0.05 mg fludrocortisone was started postoperatively.
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PMID:[Bilateral massive macronodular adrenal gland hyperplasia. A rare cause of Cushing's syndrome]. 830 53

Obesity is a multifactorial heterogenous condition. The location of excess fat on the body determines the risk of morbidity and mortality for significant disease. Visceral, or intraabdominal, fat is the fat depot most highly associated with illness and death from cardiocerebrovascular disease and diabetes. Visceral fat is also associated with a quartet of metabolic disturbances. Referred to as the metabolic syndrome, these abnormalities include hypertension, hyperlipidemia, hyperinsulinemia, and insulin resistance. The metabolic syndrome is also present in Cushing's syndrome, which is characterized by primary hypercortisolism as well as profound visceral adiposity and obesity. The interrelationship between hyperactivation or hypersensitivity of the stress axis and disease can be elucidated by an understanding of the effect of excess glucocorticoids upon energy storage and metabolism. The complex interactions of the stress axis upon the growth and reproductive axes, as well as upon the adipose tissue, suggest that chronic stress, whether psychological and/or physical, exerts an intense effect upon body composition, which, in turn, significantly affects the longevity and survival of the organism.
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PMID:Hypercortisolism and obesity. 859 40

The paper summarizes the studies documenting the outlasting of increased cardiovascular mortality in patients with Cushing's syndrome even after the hypercortisolism resolution. Despite the hypercortisolism resolution the mortality during the subsequent period of life is up to four-fold higher than in the comparable population as a whole. The pathogenesis of this cardiovascular risk is based on arterial hypertension, steroid cardiomyopathy and hyperlipidaemia with subsequent atherosclerosis. The post mortem material bears a parallel of the extent of atheromatous changes and duration of hypercorticolism. The prevention has to its disposition two mutually complementing means. The first is represented by clinical screening of hypercorticolism which enables an early recognition and therapy of the Cushing's syndrome. The successive measure resides in increased attention to the cardiovascular system even after hypercorticolism resolution. (Tab. 1, Fig. 1, Ref. 25.).
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PMID:[Cushing's syndrome is still a potentially fatal disease]. 862 39

Previous experience has shown that a non-invasive (indirect) technique using an oscillometric monitor in conjunction with a tail cuff makes routine clinical blood pressure measurement practicable in dogs. The relationship between indirect and direct readings has been evaluated in both anaesthetised and conscious dogs (Bodey and others 1994, 1996). In this study, more than 2000 pressure measurements were taken from 1903 dogs. It was found that systolic is the most variable pressure parameter and that it depends on age, breed, sex, temperament, disease state, exercise regime and, to a minor extent, diet. Diet was not a significant determinant of diastolic and mean arterial pressure. Age and breed were the major predictors for all parameters. Heart rate was primarily affected by the temperament of the animal, though other factors also play a part in prediction. The distribution of systolic, diastolic, mean arterial pressure and heart rate across the dog population approximates to a log normal distribution. On the basis of these results it is possible to describe normal ranges for canine blood pressure; definition of hypertension, though, demands attention to age and breed normal values. The existence of statistically defined hypertension in an individual or breed does not imply adverse effects justifying therapy. Among the secondary causes of hypertension, such as diabetes, obesity and hyperadrenocorticism, hepatic disease was a new addition also undocumented in humans. The hypothesis that dogs, though classic model animals for hypertension, are resistant to its development found support from the modest increase in mean pressure values observed among dogs with renal disease, notably those with substantial reduction of glomerular filtration rate. The existence of breeds such as deerhounds with average pressures in the borderline range for hypertension in humans (and many individuals, therefore, well above) suggests that dogs may also be resistant to some of the adverse effects of high blood pressure.
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PMID:Epidemiological study of blood pressure in domestic dogs. 868 54

Four dogs with thrombosis were referred for diagnostic testing and were subsequently treated by the use of streptokinase. The range of duration of clinical signs associated with thrombosis was 6 to 120 days. Causes of thrombosis were heart disease (1 dog), protein-losing nephropathy and hyperadrenocorticism (1), hyperadrenocorticism (1), and idiopathic (1). Possible factors that predisposed dogs to hypercoagulability included hypertension (2 dogs) and diabetes mellitus (1). All dogs were treated for underlying disease by use of supportive care. The first dog was treated with a loading dose of 250,000 U of streptokinase, i.v., with a subsequent maintenance dosage of 100,000 U/h, i.v., and also was treated with anticoagulant. The subsequent 3 dogs were treated with a loading dose of 90,000 U of streptokinase, i.v., and maintenance dosage of 45,000 U/ h, i.v., at various intervals. These dogs also were treated with anticoagulant. Three dogs had minor hemorrhage as an adverse effect to streptokinase infusion, but they did not require treatment for the hemorrhage. Complete resolution of the thrombus was observed in 3 dogs, and partial resolution of the thrombus was observed in the other dog. In all dogs, partial or complete resolution of clinical signs associated with thrombosis was seen. Streptokinase may be an effective treatment for dogs with thrombosis.
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PMID:Use of streptokinase in four dogs with thrombosis. 875 79

The effect of a surgical cure of hypercortisolism on hypertension in 54 patients with Cushing's syndrome was assessed. The correlation between preoperative duration of hypertension and posttreatment blood pressure was significant (P < .01). Restoration of normal cortisol was associated with blood pressure normalization in 39 out of 54 cases. Duration of hypertension of patients with normalized blood pressure was significantly shorter than that of patients with persistent hypertension postoperatively (P < .0001). Duration of hypertension, ie, long-lasting exposure to increased cortisol, appears to be the determinant of persistent hypertension following successful surgery in Cushing's syndrome.
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PMID:Effect of surgical treatment on hypertension in Cushing's syndrome. 883 10

Most patients with hypertension in the United States have essential (primary) hypertension (95%), the cause of which is unknown. The remaining 5% of adults with hypertension have the secondary form of hypertension, the cause and pathophysiologic process of which are known. Internists and other primary care physicians refer to this as treatable or curable hypertension, because the hypertension can be managed or even controlled with medications. Similarly, the condition is called surgical hypertension by surgeons in the belief that once the cause is determined and identified, surgical intervention will result in cure of hypertension. Secondary causes of hypertension include renal parenchymal disease, renovascular diseases, coarctation of the aorta, Cushing's syndrome, primary hyperaldosteronism, pheochromocytoma, hyperthyroidism, and hyperparathyroidism. Occasionally included in this category are alcohol- and oral contraceptive-induced hypertension and hypothyroidism, but these conditions are not discussed herein. The evaluation of secondary hypertension is of interest and can bring together different facets of anatomy, physiology, pharmacology, and radiology in the medical and surgical treatment of these disorders. Despite enthusiasm that can be generated in the evaluation of these conditions, evaluation can be expensive and should not be conducted for all patients with hypertension. Features that aid in the diagnosis of secondary hypertension include the following: 1. Onset of hypertension before the age of 20 or after the age of 50 years. The presence of hypertension at a young age may suggest coarctation of the aorta, fibromuscular dysplasia, or an endocrine disorder. Hypertension found for the first time after the age of 50 years may suggest the presence of renovascular hypertension caused by atherosclerosis. 2. Markedly elevated blood pressure or hypertension with severe end-organ damage, as in grade III or IV retinopathy. These findings suggest the presence of renovascular hypertension or pheochromocytoma. 3. Specific body habitus and ancillary physical findings. For example, truncal obesity and purple striae occur with hypercortisolism, and exophthalmos is associated with hyperthyroidism. 4. Resistant or refractory hypertension (poor response to medical therapy usually necessitating use of more than three antihypertensive medications from three different classes). 5. Specific biochemical test that suggest the existence of certain disorders, such as hypercalcemia in hyperparathyroidism, hyperglycemia in Cushing's syndrome and pheochromocytoma, and unprovoked hypokalemia with renin-producing tumors, primary hyperaldosteronism, or renin-mediated renovascular hypertension. 6. Other characteristics that may suggest secondary hypertension such as abdominal diastolic bruits (renovascular hypertension), decreased femoral pulses (coarctation of the aorta), or bitemporal hemianopias (Cushing's disease). A combination of a good history and physical examination, astute observation, and accurate interpretation of available data usually are helpful in the diagnosis of a specific causation.
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PMID:Secondary hypertension: evaluation and treatment. 894 19

Cushing's disease and empty sella without evidence of pituitary adenoma are rarely observed. To our knowledge, there is very little documentation on long-term therapeutic follow-up with the steroidogenesis inhibitor ketoconazole. A 48-year-old woman with uncontrolled insulin-dependent diabetes mellitus, severe hypertension, and clinical findings of hypercortisolism was referred to our hospital. Endocrine evaluation of adrenocortical function evidenced hypothalamic-pituitary-hypercortisolism, and excluded adrenal tumor or an ectopic corticotropin source. Magnetic resonance imaging disclosed an empty sella turcica but not pituitary adenoma. The patient was treated with a steroidogenesis inhibitor, ketoconazole (600 mg daily) which reduced urinary cortisol excretion to within the normal range. Serum cortisol levels also returned to normal in the morning but not in the evening. The patient has continued on ketoconazole therapy for the past 7 years, with neither side effects nor tachyphylaxis. The reduction of cortisol secretion brought about significantly improved control of diabetes mellitus and hypertension, although signs of hypercortisolism have persisted. Radiographic studies of the hypophysis during follow-up have not evidenced adenoma.
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PMID:[Cushing's disease associated with empty sella: a clinical case treated for years with ketoconazole]. 907 69

Carbohydrate and lipid metabolism was cross-sectionally assessed in 16 patients with endogenous hypercortisolism (endogenous Cushing syndrome). Five patients (31%) had fasting glucose levels over 6.6 mmol/l and a HbA1C over 7.5%. Six patients (38%) had diabetes mellitus based on an abnormal 75 g oral glucose tolerance test (OGTT) and two additional patients (13%) had impaired glucose tolerance based on an OGTT. Compared to obese individuals, patients with Cushing syndrome had an elevated glucose but no elevated insulin response to the OGTT. Regression analysis showed positive correlations between 24-h urinary free cortisol (UFC) and fasting blood glucose (P < 0.0005), UFC and OGTT glucose area under the curve (AUC) (P < 0.01), and UFC and HbA1C (P < 0.005). UFC levels were negatively correlated (P < 0.05) with OGTT insulin AUC and insulin/glucose ratios. Eleven (69%) patients required anti-hypertensive therapy for blood pressure control. Total cholesterol and triglycerides were elevated in patients with Cushing syndrome compared to obese controls, while LDL and HDL cholesterol, and Lp(a) were similar in the two groups. We conclude that impaired glucose tolerance and/or diabetes in patients with endogenous Cushing syndrome is due to the hyperglycemic effects of cortisol with relative insulinopenia. Thus, Cushing syndrome shares features with both the Metabolic Syndrome X and NIDDM, including impaired glucose uptake, hyperlipidemia and hypertension. However, in Cushing syndrome, a relative insulinopenia occurs, while in Metabolic Syndrome X and NIDDM, insulin excess is observed. In Cushing syndrome, as the hypercortisolemia exacerbates, insulinopenia becomes more paramount, suggesting that cortisol exerts a direct or indirect "toxic" effect on the beta-cell.
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PMID:Carbohydrate and lipid metabolism in endogenous hypercortisolism: shared features with metabolic syndrome X and NIDDM. 907 4


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