Hypertension dexamethasone

We describe below the use of halloysite nanotubules for entrapment and the subsequent release of three drugs Nifedipine (anti-anginal), Furosemide (anti-hypertension and diuretic), and Dexamethasone (synthetic corticosteroid). To increase the loading of these poorly soluble drugs in the tubules, we loaded them into a water-alcohol co-solvent solution (0, 10, and 50% ethanol). 

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 effects of topical dexamethasone on intraocular pressure have been compared with those of fluorometho-lone (SEDA-22, 446 66). The ocular hypertensive response to topical dexamethasone in children occurs more often, more severely, and more rapidly than that reported in adults. It should be avoided in children if possible and it is desirable to monitor the intraocular pressure when it is being used. Fluorometholone may be more acceptable. 

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). 

Corticosteroid-induced ocular hypertension appears to relate not only to the individual patient but to the specific steroid used. In general, dexamethasone 0.1%, betamethasone 0.1%, and prednisolone acetate appear more likely to induce significant lOP elevations than do fluorometholone alcohol and medrysone. Clinical studies with rimexolone and LE indicate that they have less potential to elevate lOP than does dexamethasone phosphate or prednisolone acetate. 

Albendazole has sometimes aggravated extrapyramidal disorders or precipitated seizures in patients with prior epileptic symptoms. The risk of intracranial hypertension has led some to suggest that glucocorticoids should be given preventively when using albendazole in neurocysticercosis (24) however, dexamethasone can interact with albendazole, increasing its plasma concentrations (25), and it is not clear whether this might produce new problems. 

A 32-year-old woman presents to her obstetrician/gynecologist with complaints of irregular periods, hirsutism, and mood swings. She also reports weight gain and easy bruising. On examination, she is found to have truncal obesity, a round moon face, hypertension, ecchymoses, and abdominal striae. The patient is given a dexamethasone suppression test which reveals an elevated level of cortisol. 

A 45-year-old female patient presents with hirsutism, striae, bruising, acne, and hyperpigmentation of the skin. After a thorough physical examination the physician notes that she also suffers from hypertension and shows signs of a buffalo hump on her back between the shoulders. Cushing syndrome is snspected and after laboratory tests show elevated blood cortisol levels she is given a dexamethasone suppression test. Her resnlts are positive. 

Bramlage CP, Schlumbohm C, Pryce CR et al (2009) Prenatal dexamethasone exposure does not alter blood pressure and nephron number in the young adult marmoset monkey. Hypertension 54 1115-1122... 

Glucocorticoid resistance is characterized by high levels of cortisol (without stigmata of Cushing syndrome), resistance of the hypothalamic-pituitary-adrenal axis to dexamethasone, and an affinity defect of the glucocorticoid receptor. Some of the affected patients presented with hypertension and hypokalemia due to illegal activation of the mineralocorticoid receptor by cortisol [16]. 

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