Hypertension glucocorticoids

Cortisol-Cortisone Conversion. Under normal conditions, this equilibrium slightly favors the oxidized compound. Similarly, the conversion of corticosterone to 11-deoxycorticosterone is also mediated by the liP-hydroxysteroid dehydrogenase enzyme system and requites NAD(P) /NAD(P)H. This conversion is especially important both in the protection of the human fetus from excessive glucocorticoid exposure, and in the protection of distal nephron mineral ocorticoid receptors from glucocorticoid exposure (14). The impairment of this conversion is thought to result in hypertension associated with renal insufficiency (15). 

The glucocorticoids are administered with caution to patients with renal or hepatic disease hypothyroidism, ulcerative colitis, diverticulitis, peptic ulcer disease, inflammatory bowel disease hypertension, osteoporosis, convulsive disorders, or diabetes. The glucocorticoids... 

Maoris N. Glucocorticoid use and risks of ocular hypertension and glaucoma. 

The well-appreciated adverse effects of glucocorticoids include hyperglycemia, hypertension, osteoporosis, fluid retention and electrolyte disturbances, myopathies, psychosis, and reduced resistance to infection. In addition, glucocorticoid use may cause adrenocortical suppression. Specific regimens for withdrawal of glucocorticoid therapy have been suggested. 

Steroids have mineralocorticoid and glucocorticoid effects. Betamethasone has little, if any, mineralocorticoid effect. However, it should be used with caution in patients predisposed to hypertension since mineralocorticoid effects may lead to sodium and water retention and an increase in blood pressure. When used systemically, especially at high doses, steroid therapy is associated with a risk of psychiatric reactions such as euphoria, irritability, mood lability and sleep disorders. Glucocorticoid side-effects include diabetes and osteoporosis. 

IV.a.1.3. Hypertension. Excess glucocorticoids can lead to increased blood pressure. These effects contribute to increased risk of heart-related illness... 

IV.a.1.11. Mineralocorticoid side effects. These are common problems, causing sodium and water retention, hypokalaemia and hypertension. They are often marked with hydrocortisone, but may be seen with high doses of all of the therapeutic glucocorticoid drugs. 

The first point is that treatment with steroids is generally palliative rather than curative, and only in a very few diseases, such as leukemia and nephrotic syndrome, do corticosteroids alter prognosis. One must also consider which is worse, the disease to be treated or possible induced hypercortisolism. The patient s age can be an important factor, since such adverse effects as hypertension are more apt to occur in old and infirm individuals, especially in those with underlying cardiovascular disease. Glucocorticoids should be used with caution during pregnancy. If steroids are to be employed, prednisone or prednisolone should be used, since they cross the placenta poorly. 

Glucocorticoids induce cataract formation, particularly in patients with rheumatoid arthritis. An increase in intraocular pressure related to a decreased outflow of aqueous humor is also a frequent side effect of periocular, topical, or systemic administration. Induction of ocular hypertension, which occurs in about 35% of the general population after glucocorticoid administration, depends on the specific drug, the dose, the frequency of administration, and the glucocorticoid responsiveness of the patient. 

Edema Induced by glucocorticoids Hypertension with or without edema Ascites Glaucoma... 

Patients receiving glucocorticoids must be monitored carefully for the development of hyperglycemia, glycosuria, sodium retention with edema or hypertension, hypokalemia, peptic ulcer, osteoporosis, and hidden infections. 

Glucocorticoids must be used with great caution in patients with peptic ulcer, heart disease or hypertension with heart failure, certain infectious illnesses such as varicella and tuberculosis, psychoses, diabetes, osteoporosis, or glaucoma. 

Antagonists of glucocorticoid and mineral ocorticoid activity have found increased use clinically in the treatment of hypertension, Cushing s disease, and heightened intraocular pressure. 

A study has been undertaken to clarify whether glucocorticoid excess affects endothelium-dependent vascular relaxation in glucocorticoid treated patients and whether dexamethasone alters the production of hydrogen peroxide and the formation of peroxynitrite, a reactive molecule between nitric oxide and superoxide, in cultured human umbilical endothelial cells (7). Glucocorticoid excess impaired endothelium-dependent vascular relaxation in vivo and enhanced the production of reactive oxygen species to cause increased production of peroxynitrite in vitro. Glucocorticoid-induced reduction in nitric oxide availability may cause vascular endothelial dysfunction, leading to hypertension and atherosclerosis. 

The benefit of glucocorticoid therapy is often limited by several adverse reactions, including cardiovascular disorders such as hypertension and atherosclerosis. Plasma volume expansion due to sodium retention plays a minor role, but increased peripheral vascular resistance, due in part to an increased pressor response to catecholamines and angiotensin II, plays a major role in the pathogenesis of hypertension induced by glucocorticoid excess. However, the molecular mechanism remains unclear. 

The secondary mineralocorticoid activity of glucocorticoids can lead to salt and water retention, which can cause hypertension. Although the detailed mechanisms are as yet uncertain, glucocorticoid-induced hypertension often occurs in elderly patients and is more common in patients with total serum calcium concentrations below the reference range and/or in those with a family history of essential hypertension (SEDA-20, 368 19). 

Long-term glucocorticoid treatment can result in papilledema and increased intracranial pressure (the syndrome of pseudotumor cerebri or so-called benign intracranial hypertension ), particularly in children. 

A 6-year-old girl, who had taken prednisone for 2.5 years for nephrotic syndrome with seven relapses in 3 years, developed symptoms of benign intracranial hypertension after oral glucocorticoid dosage reduction over 10 months from 30 mg/day to 2.5 mg/every other day (46). Laboratory studies and head CT scan were normal, but there was bilateral papilledema and the cerebrospinal fluid pressure was increased. She was given prednisone 1 mg/kg/day initially, with acetazola-mide, and 25 ml of cerebrospinal fluid was removed. All her symptoms resolved and treatment was gradually withdrawn. She developed no further visual failure. 

Ocular hypertension and open-angle glaucoma are well-known adverse effects of ophthalmic administration of glucocorticoids (SEDA-17, 449). 

Glaucoma and ocular hypertension have been reported after dermal application of glucocorticoids for facial atopic eczema (SEDA-19,376) (64), and after treatment with beclomethasone by nasal spray and inhalation (SEDA-20, 373 65). 

Children have more frequent, more severe, and more rapid ocular hypertensive responses to topical dexamethasone than adults. In one case a systemic glucocorticoid caused significant but asymptomatic ocular hypertension in a child (67). 

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