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

Mortality rates are increased in acromegaly. previous studies have shown that growth hormone and insulin-like growth factor 1 levels, male gender,age, hypertension, delayed diagnosis and prior pituitary radiotherapy are independent predictors of increased mortality. A new study by Sherlock et al. now adds adrenal insufficiency and hydrocortisone replacement dose to the list of independent predictors of acromegaly-associated mortality.
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PMID:Pituitary gland: predictors of acromegaly-associated mortality. 2009 46

Abiraterone acetate (CB7630), a pregnenolone analog, is an orally administered small molecule that irreversibly inhibits a rate-limiting enzyme in androgen biosynthesis, CYP17, and blocks the synthesis of androgens in the testes, adrenal glands and prostate without causing adrenal insufficiency. In clinical studies, abiraterone acetate is well tolerated and shows promising clinical activity in castration-resistant prostate cancer. The recommended Phase II dose of abiraterone acetate is 1000 mg orally daily in combination with prednisone 5 mg twice daily. Side effects are minimal and mostly associated with secondary mineralocorticoid excess, owing to a compensatory increase in upstream steroids, such as deoxycorticosterone and corticosterone. These include hypertension, hypokalemia and edema and are easily manageable with a selective mineralocorticoid antagonist, such as eplerenone, or low-dose corticosteroids. Currently, abiraterone acetate is being tested in a Phase III trial for men with progressive castration-resistant prostate cancer who are chemotherapy naive. A Phase III trial for patients following prior chemotherapy has been completed and is awaiting analysis.
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PMID:Abiraterone acetate: a promising drug for the treatment of castration-resistant prostate cancer. 2046 82

Although veterinary clinicians commonly rely on panels of laboratory tests with individual results flagged when abnormal, care should be taken in interpreting normal test results as well. There are several examples of this in evaluating patients with endocrine disease. The finding of a normal leukogram (absence of a stress leukogram) can be indicative of adrenal insufficiency in dogs, and this disorder can be especially elusive when there are no overt indicators of mineralocorticoid deficiency. Cats with hyperthyroidism can have normal serum thyroid hormone concentrations, normal hematocrits, and normal serum concentrations of creatinine despite the presence of disease that affects these parameters. A normal serum phosphorus concentration, in the face of azotemia, isosthenuria, and hypertension can point a clinician toward a diagnosis of primary hyperaldosteronism rather than primary renal disease. A normal serum parathyroid hormone concentration in the face of hypercalcemia is inappropriate and can indicate the presence of primary hyperparathyroidism. Similarly, hypoglycemia accompanied by a normal serum insulin concentration can be found in cases of hyperinsulinism. These normal findings in abnormal patients, and their mechanisms, are reviewed.
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PMID:When normal is abnormal: keys to laboratory diagnosis of hidden endocrine disease. 2159 44

Benign intracranial hypertension (Pseudotumor cerebri) has been described as related to the reduction in steroid levels in Cushing's disease (CD), especially after surgical remission. Ketoconazole is a common and effective adjuvant therapy for hypercortisolism, but the major concern is liver enzyme dysfunction. We describe here the case of a 12-year old girl with CD who developed benign intracranial hypertension during treatment with ketoconazole. She presented headache, vomiting, a black spot on her right temporal visual field, and signs of elevated intracranial pressure. Pituitary image was normal on magnetic resonance image (MRI), and all symptoms improved after treatment with acetazolamide. We call attention to the diagnosis of this disorder in CD patients, especially children on ketoconazole treatment, because it could be confounded with adrenal insufficiency and lead to definitive severe visual impairment.
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PMID:Pseudotumor cerebri during Cushing's disease treatment with ketoconazole. 2177 32

Preoperative preparation of the patients with adrenal cortex dysfunction is based on the careful preoperative evaluation of the type and the severity of the disturbance. The dysfunction involving adrenal glands may be: insufficiency (severe, mild, expressed) and hyperfunction (hypercorticism and/or hyperaldosteronism). If we speak about the patients with limited adrenal reserve (Addison's disease, therapeutic glucocorticoid application etc.) they need necessary corticosteroid supplementation, during preoperative preparation, as well as, during complete perioperative period. Doses needed for the substitution are adjusted according to the severity of adrenal insufficiency and according to the extent of the planned surgical procedure. Patients with Cushing's syndrome (or other form of hypercorticism), as well as, patients with Conn's syndrome (or other forms of hyperaldosteronism), do have numerous organ dysfunctions, that are significant in preoperative preparation, anesthesia and for the outcome of the surgical treatment. Common feature for both of the above syndromes is hydroelectrolyte disbalance, with hypokalemia, metabolic alkalosis and hypertension. Disturbances related to the adrenal cortex hyperfunction must be corrected preoperatively, in order to avoid complications. When we speak about hypokalemia it must be promptly corrected even before urgent/vital surgical procedure because it may cause severe intraoperative cardiac arrhythmia.
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PMID:Contemporary approach to preoperative preparation of patients with adrenal cortex hormones dysfunction. 2187 60

Skin-lightening cosmetics are used by many women and men around the world. The products contain a variety of substances, which are often unknown to the users. Most of these products include topical corticosteroids, hydroquinone and mercury salts. Many other substances may be added. Several surveys and cohort studies, including several thousand individuals, have shown that regular application of skin-lightening cosmetics to large surface areas can have irreversible cutaneous adverse effects, such as patchy hyper- or hypopigmentation, skin atrophy, stretch marks and delayed wound healing, and can also mask or, on the contrary, promote or reactivate skin infections. Cases of skin cancer have been attributed to skin-lightening cosmetics. A Senegalese cohort study of 147 women showed a statistically significant increase in the risk of hypertension and diabetes linked to the use of skin-lightening agents. Other systemic adverse effects attributed to skin-lightening cosmetics include Cushing's syndrome, adrenal insufficiency, nephrotic syndrome, neurological disorders, and ocular disorders. Hypersensitivity reactions, including anaphylaxis, have also been attributed to these products. Many skin-lightening cosmetics contain substances that can harm the unborn child. For example, tretinoin is teratogenic while salicylic acid is feto-toxic. In practice, users are often unaware of the risk of severe adverse effects associated with skin-lightening cosmetics. Users should be informed of these adverse effects and encouraged to stop using these products, especially when skin disorders appear.
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PMID:Skin-lightening cosmetics: frequent, potentially severe adverse effects. 2195 16

Lipoid congenital adrenal hyperplasia (lipoid CAH), a rare disorder of steroid biosynthesis, is the most severe form of CAH. In this disorder the synthesis of glucocorticoids, mineralocorticoids and sex steroids is impaired which result in adrenal failure, severe salt wasting crisis and hyperpigmentation in phenotypical female infants irrespective of genetic sex. In this report, we presented a 28-day-old phenotypic female infant, which referred with lethargy, failure to thrive and electrolyte abnormalities. Considering the clinical and biochemical findings, lipoid CAH was diagnosed and replacement therapy with standard doses of glucocorticoid and mineralocorticoid and sodium chloride was initiated. During follow-up, she had good clinical condition, but at 6 years of age, she refers with hypertension and adrenal insufficiency because of arbitrary drug discontinuation by mother. In ultrasonography an abdominal mass (the testicles) was reported. Chromosome study showed 46XY pattern. Orchiectomy was performed. We recommended that in cases with clinical presentation of adrenal insufficiency if there is not the facility to determine the karyotype, repeated ultrasonography perform during follow-up. In addition, investigating the genetic bases of the disorder would help us to determine the pathogenesis of lipoid CAH in our community. It would be helpful in prenatal diagnosis and treatment of the disorder to prevent its related comorbidities.
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PMID:A case of congenital lipoid adrenal hyperplasia. 2289 Nov 54

Blockade of the renin-angiotensin-aldosterone system (RAAS) is an established method to lower blood pressure in patients with hypertension. Aldosterone, the end product of the RAAS cascade, acts by increasing salt reabsorption in the kidney and catecholamine release from the adrenal medulla. Currently available aldosterone inhibitors have the disadvantage of increasing circulating aldosterone and thus may lead to aldosterone breakthrough. Aldosterone synthase inhibition (ASI) is a novel approach to suppressing the RAAS. Due to homology between the enzymes responsible for aldosterone synthesis (CYP11B2) and cortisol synthesis (CYP11B1), the blockade of aldosterone synthesis may also suppress cortisol release. The authors evaluated the effect of the novel ASI LCI699 on the cortisol response to adrenocorticotropic hormone (ACTH) stimulation in patients with hypertension in order to find the maximally tolerated dose (MTD) in this patient population. Among the 63 patients evaluated, there was a dose- and time-dependent effect of LCI699 on both aldosterone and ACTH-stimulated cortisol. Based on exposure-response analysis, the MTD was estimated to be 1.30 mg once daily with a 90% prediction interval of 0.88 mg once daily to 1.81 mg once daily. No patients required intervention for adrenal insufficiency. LCI699 was well tolerated with no serious adverse events.
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PMID:The effects of aldosterone synthase inhibition on aldosterone and cortisol in patients with hypertension: a phase II, randomized, double-blind, placebo-controlled, multicenter study. 2294 55

There are few published data on aldosterone and cortisol co-secreting adrenal tumours. Failure to perform comprehensive preoperative endocrine investigations in patients with adrenal "incidentalomas" or in those thought to be secreting only one hormone may account for this. Clinically patients with such lesions may have evidence of hypertension and hypokalaemia with no features of cortisol excess. Preoperative diagnosis of such lesions with accurate endocrinological work up is essential to prevent adrenal insufficiency and haemodynamic crises following removal of such glands. We present a series of 4 patients with co-secreting tumours treated by laparoscopic adrenalectomy between September 2010 and March 2011. Our experience suggests that dual secretors are more common than originally thought. A high index of suspicion and adequate endocrine work up is paramount in diagnosing such tumours and in experienced hands, laparoscopic adrenalectomy with appropriate substitutive steroid cover is safe, feasible and curative for these functioning adrenal tumours.
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PMID:Laparoscopic adrenalectomy for co-secreting aldosterone and cortisol adenomas. 2295 68

Autoimmune polyendocrine syndrome type II (APS-II) is the most common immunoendocrinopathy syndrome. APS-II is defined by the development of two or more of the following entities: primary adrenal insufficiency (Addison's disease), Graves' disease, type 1A diabetes mellitus, autoimmune thyroiditis, primary hypogonadism, celiac disease, and myasthenia gravis. Other frequent clinical findings are vitiligo, alopecia, pernicious anemia and/or serositis. Primary adrenal insufficiency in these patients affects the adrenal cortex, which is destroyed by autoantibodies against 21-hydroxylase. Unlike other causes of adrenal insufficiency (infectious diseases, infiltrative diseases, bleeding, tumors), the adrenal medulla is not involved. Pheochromocytomas are tumors arising from the chromaffin cells of the sympathetic nervous system in the adrenal medulla. The clinical symptoms of these tumors vary from isolated hypertension or hypertension accompanied by paroxysmal episodes -including the classical triad of headache, palpitations and diaphoresis-to potentially serious manifestations such as acute pulmonary edema, arrhythmias and sudden death. Nevertheless, up to 40% of affected patients are asymptomatic. We present the case of a patient diagnosed with APS-II who developed a pheochromocytoma. In this patient, the adrenal gland cortex was atrophied and the tumor was attached to the adrenal medulla. This coexistence of endocrinopathies, with no etiologic connection, is a surprising finding, which has not previously been described in the current literature.
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PMID:An unusual association: pheochromocytoma on an atrophied adrenal gland due to addison's disease. 2298 Apr 66


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