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Losing fat deposits caused by prednisone

What Is the Connection between Prednisone and Weht Day 1: 10 mg PO before breakfast, 5 mg after lunch and after dinner, and 10 mg at bedtime Day 2: 5 mg PO before breakfast, after lunch, and after dinner and 10 mg at bedtime Day 3: 5 mg PO before breakfast, after lunch, after dinner, and at bedtime Day 4: 5 mg PO before breakfast, after lunch, and at bedtime Day 5: 5 mg PO before breakfast and at bedtime Day 6: 5 mg PO before breakfast Immediate-release: ≤10 mg/day PO added to disease-modifying antirheumatic drugs (DMARDs) Delayed-release: 5 mg/day PO initially; maintenance: lowest dosage that maintains clinical response; may be taken at bedtime to decrease morning stiffness with rheumatoid arthritis Take with meal or snack Hh-dose glucocorticoids may cause insomnia; immediate-release formulation is typiy administered in morning to coincide with circadian rhythm Delayed-release formulation takes about 4 hours to release active substances; thus, with this formulation, timing of dose should take into account delayed-release pharmacokinetics and disease or condition being treated (eg, may be taken at bedtime to decrease morning stiffness with rheumatoid arthritis) Allergic: Anaphylaxis, angioedema Cardiovascular: Bradycardia, cardiac arrest, cardiac arrhythmias, cardiac enlargement, circulatory collapse, congestive heart failure, fat embolism, hypertension, hypertrophic cardiomyopathy in premature infants, myocardial rupture after recent myocardial infarction, pulmonary edema, syncope, tachycardia, thromboembolism, thrombopebitis, vasculitis Dermatologic: Acne, allergic dermatitis, cutaneous and subcutaneous atrophy, dry scalp, edema, facial erythema, hyper- or hypopmentation, impaired wound healing, increased sweating, petechiae and ecchymoses, rash, sterile abscess, striae, suppressed reactions to skin tests, thin fragile skin, thinning scalp hair, urticaria Endocrine: Abnormal fat deposits, decreased carbohydrate tolerance, development of cushingoid state, hirsutism, manifestations of latent diabetes mellitus and increased requirements for insulin or oral hypoglycemic agents in diabetics, menstrual irregularities, moon facies, secondary adrenocortical and pituitary unresponsiveness (particularly in times of stress, as in trauma, surgery, or illness), suppression of growth in children Fluid and electrolyte disturbances: Fluid retention, potassium loss, hypertension, hypokalemic alkalosis, sodium retention Gastrointestinal: Abdominal distention, elevation of serum liver enzymes levels (usually reversible upon discontinuance), hepatomegaly, hiccups, malaise, nausea, pancreatitis, peptic ulcer with possible perforation and hemorrhage, ulcerative esophagitis General: Increased appetite and weht gain Metabolic: Negative nitrogen balance due to protein catabolism Musculoskeletal: Osteonecrosis of femoral and humeral heads, Charcot-like arthropathy, loss of muscle mass, muscle weakness, osteoporosis, pathologic fracture of long bones, steroid myopathy, tendon rupture, vertebral compression fractures Neurologic: Arachnoiditis, convulsions, depression, emotional instability, euphoria, headache, increased intracranial pressure with papilledema (pseudotumor cerebri; usually following discontinuance of treatment), insomnia, meningitis, mood swings, neuritis, neuropathy, paraparesis/paraplegia, paresthesia, personality changes, sensory disturbances, verto Ophthalmic: Exophthalmos, glaucoma, increased intraocular pressure, posterior subcapsular cataracts, central serous chorioretinopathy Reproductive: Alteration in motility and number of spermatozoa Untreated serious infections Documented hypersensitivity Varicella Administration of live or attenuated live vaccine (Advisory Committee on Immunization Practices (ACIP) and American Academy of Family Physicians (AAFP) state that administration of live virus vaccines usually is not contraindicated in patients receiving corticosteroid therapy as short-term ( Monitor for hypothalamic-pituitary-adrenal (HPA) axis suppression, Cushing syndrome, and hyperglycemia Prolonged use associated with increased risk of infection; monitor Use with caution in cirrhosis, ocular herpes simplex, hypertension, diverticulitis, hypothyroidism, myasthenia gravis, peptic ulcer disease, osteoporosis, ulcerative colitis, psychotic tendencies, renal insufficiency, pregnancy, diabetes mellitus, congestive heart failure, thromboembolic disorders, GI disorders Long-term treatment associated with increased risk of osteoporosis, myopathy, delayed wound healing Patients receiving corticosteroids should avoid chickenpox or measles-infected persons if unvaccinated Latent tuberculosis may be reactivated (patients with positive tuberculin test should be monitored) Some suggestion (not fully substantiated) of slhtly increased cleft palate risk if corticosteroids are used in pregnancy Methylprednisolone is preferred in hepatic impairment because prednisone must be converted to prednisolone in liver Prolonged corticosteroid use may result in elevated intraocular pressure, glaucoma, or cataracts May cause impairment of mineralocorticoid secretion; administer mineralocorticoid concomitantly May cause psychiatric disturbances; monitor for behavioral and mood changes; may exacerbate pre-existing psychiatric conditions Monitor for Kaposi sarcoma Pregnancy category: C (immediate release); D (delayed release) Drug may cause fetal harm and decreased birth weht; maternal corticosteroid use during first trimester increases incidence of cleft lip with or without cleft palate Lactation: Of maternal serum metabolites, 5-25% are found in breast milk; not recommended, or, if benefit outwehs risk, use lowest dose Glucocorticosteroid; elicits mild mineralocorticoid activity and moderate anti-inflammatory effects; controls or prevents inflammation by controlling rate of protein synthesis, suppressing mration of polymorphonuclear leukocytes (PMNs) and fibroblasts, reversing capillary permeability, and stabilizing lysosomes at cellular level; in physiologic doses, corticosteroids are administered to replace deficient endogenous hormones; in larger (pharmacologic) doses, they decrease inflammation The above information is provided for general informational and educational purposes only. What Is the Connection between <b>Prednisone</b> and Weht
The fat distribution seen with prednisone is not preventable. The extent of redistribution can vary, and [email protected] No, I don't think so. Prednisone does cause water retention but it also causes weht gain. It's been six months and I'm still struggling to lose weht I gained on prednisone.

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Prednisone & Belly Fat. soontobeskinnysara Posts 177Member Member Posts 177Member Member. Hi, You should check out smack fat its a amazing community that strives on helping & suggesting solutions to losingI've taken prednisone before and it causes me to bloat up majorly.

Why Do People Gain Weht on Prednisone? LIVESTRONG. COM By Janet Segall, IPPF Executive Director In order for patients with pemphus and pemphoid to get control of their disease, there are certain drugs that patients must take. Why Do People Gain Weht on <strong>Prednisone</strong>? LIVESTRONG. COM
Prednisone not only causes weht gain, it can result in a phenomenon. This means fat deposits collect in unusual areas, such as the back or base of. decreasing your dosage, which can reduce the redistribution effect.

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Prednisone is an effective treatment, but long-term use can cause side effects. Other common prednisone side effects with long-term use include acne, weht gain, fatty deposits in the face, thinning skin and stretch marks.

Moon Facies Causes and Treatment - WebMD If your face has gradually swollen into a rounded shape, you may have moon facies. Moon Facies Causes and Treatment - WebMD
Moon facies may cause the face to gradually become round, full. Fat deposits in the sides of the skull can also make the face look. Long-term use of steroid medications like prednisone for conditions. Weht Loss Tips.

Losing fat deposits caused by prednisone:

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