Why do corticosteroids cause moon face

Corticosteroids (glucocorticoids), used frequently as potent anti-inflammatory agents, increase the risk of glaucoma by raising the intraocular pressure (IOP) when administered exogenously (topically, periocularly or systemically) and in certain conditions of increased endogenous production (. Cushing's syndrome). Approximately 18 to 36% of the general population are corticosteroid responders. This response is increased to 46 to 92% in patients with primary open-angle glaucoma (POAG). Patients over 40 years of age and with certain systemic diseases (. diabetes mellitus, high myopia) as well as relatives of patients with POAG are more vulnerable to corticosteroid-induced glaucoma. The association of corticosteroid-induced ocular hypertension in other conditions which are considered as risk factors for glaucoma (racial origins, hypertension, migraine, vasospasm) is likely but not fully established. The proposed mechanism of corticosteroid-induced glaucoma includes morphological and functional changes in the trabecular meshwork system and is similar to the pathogenesis of POAG. Trabecular cells exposed to corticosteroids in vitro show endoreplication of nuclei, an increase in cell size and excessive production of an approximately 56kD glycoprotein, identified as myocilin and transcribed by the GLC1A gene. Induction of ocular hypertension after corticosteroid administration depends on the specific drug, the dose, the frequency of administration and the corticosteroid responsiveness of the patient. The risk of corticosteroid-induced glaucoma can be minimised with judicious use of corticosteroids, as well as education of patients and medical practitioners. New treatment modalities include modified steroids and nonsteroidal anti-inflammatory agents that will have less effect on the elevation of IOP.

The NIAMS gratefully acknowledges the assistance of the following individuals in the preparation and review of previous versions of this publication: Gayle Lester, ., Joan McGowan, ., James Panagis, ., Susana Serrate-Sztein, ., and Bernadette Tyree, ., NIAMS/NIH; Kenneth D. Brandt, ., Indiana University School of Medicine, Indianapolis, IN; Victor M. Goldberg, ., University Hospitals of Cleveland, OH; Marc C. Hochberg, ., ., University of Maryland, Baltimore, MD; John Klippel, ., Arthritis Foundation, Atlanta, GA; and Roland Moskowitz, ., Case Western Reserve University, Cleveland, OH. Special thanks also go to the patients who reviewed this publication and provided valuable input.

Certain drugs such as troleandomycin (TAO), erythromycin ( Ery-Tab , EryPed 200), and clarithromycin ( Biaxin ) and ketoconazole ( Nizoral ) can reduce the ability of the liver to metabolize (breakdown) corticosteroids and this may lead to an increase in the levels and side effects of corticosteroids in the body. On the other hand, phenobarbital, ephedrine , phenytoin ( Dilantin ), and rifampin ( Rifadin , Rimactane ) may reduce the blood levels of corticosteroids by increasing the breakdown of corticosteroids by the liver. This may necessitate an increase of corticosteroid dose when they are used in combination with these drugs.

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In pregnancy, pharmacokinetics of corticosteroids changes. Systemic corticosteroids are not teratogenic. Pregnant women receiving corticosteroid therapy suffer the same side effects and benefits as do treated women who are not pregnant. Clinical experience suggests no abnormalities of children of mothers treated with usual doses of prednisone and methylprednisolone throughout pregnancy, but premature rupture of amniotic membranes and low birthweight babies may occur. Betamethasone and dexamethasone are used to treat the fetus. The effect on the fetus of bolus doses of methylprednisolone is unknown. Very little corticosteroid ingested by the mother enters her breast milk. Corticosteroid therapy in pregnancy is appropriate to control clinically active maternal illness; to treat an in utero infant suffering from neonatal lupus-associated carditis; in stress doses (in corticosteroid-treated patients) for labor and delivery: and, pre-delivery, to induce fetal lung maturation.

Why do corticosteroids cause moon face

why do corticosteroids cause moon face

I know I have had a fatty liver for years. Recently I had a test for my AMAs ( antimitrochrondrial antibodies) which were high and a marker for primary biliary cirrhosis . So I consented to a liver biopsy which showed mild inflammation and higher scarring and no PBC!
The doctor brushed off Milk Thistle which I swore by for 17 years. I think my inflammation is low. He said to work on diet and exercise, so I am glad to find this site. I always wondered if having Lyme Disease scarred my liver as the tick bit me near my liver and I was very sick.

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