Nursing Implicat: Ion: Indication: Action
Nursing Implicat: Ion: Indication: Action
Nursing Implicat: Ion: Indication: Action
Reactions journal: "In conclusion, our data show that in a cohort of patients with severe aplastic anemia receiving
immunosuppressive therapy, telomere length was not associated with response but was associated with risk of
relapse, clonal evolution, and overall survival."
Generic Name for Prednisone
Legal Classification:
Rx
Glucocorticoid.
Manufacturer of Prednisone
Corticosteroid-responsive disorders.
Tuberculosis. Latent amebiasis. Strongyloides infestation. Hypothyroidism. Ocular herpes simplex. Cirrhosis. Renal
insufficiency. If exposed to chickenpox or measles, consider prophylactic passive immune therapy. Ulcerative colitis
if perforation pending. Peptic ulcer. Diverticulitis. Intestinal anastomoses. Myasthenia gravis. Hypertension.
Osteoporosis. Diabetes. Kaposi's sarcoma. Supplement with additional steroids in physiologic stress. Avoid abrupt
cessation. May increase risk and mask signs of infection. May cause electrolyte imbalances, adrenocortical
insufficiency, psychotic derangements. Alternate, intermittent, or single-daily doses at 8AM minimize adrenal
suppression. Use lowest effective dose. Monitor weight, growth, fluid and electrolyte balance. Pregnancy. Nursing
mothers.
Barbiturates, hydantoins, rifampin, other hepatic enyzme inducers may decrease effects. Potentiated by
ketoconazole, troleandomycin. Excretion of high-dose aspirin increased. Caution with diuretics, digoxin, aspirin in
hypoprothrombinemia. Potentiated by oral contraceptives. Monitor oral anticoagulants.
HPA axis suppression, increased susceptibility to infection, glaucoma, cataracts, secondary infections, hypokalemia,
hypocalcemia, hypernatremia, hypertension, CHF, psychic disorders, myopathy, osteoporosis, peptic ulcer, dermal
atrophy, increased intracranial pressure, carbohydrate intolerance.
How is Prednisone supplied?Contact supplier.Related Disease:
Corticosteroid-responsive disorders
Mechanism of Action: Glucocorticoids are naturally occurring hormones that prevent or suppress inflammation and
immune responses when administered at pharmacological doses. At a molecular level, unbound glucocorticoids
readily cross cell membranes and bind with high affinity to specific cytoplasmic receptors. This binding induces a
response by modifying transcription and, ultimately protein synthesis to achieve the steroid's intended action. Such
actions may include: inhibition of leukocyte infiltration at the site of inflammation, interference in the function of
mediators of inflammatory response, and suppression of humoral immune responses. Some of the net effects include
reduction in edema or scar tissue, as well as a general suppression in immune response. The degree of clinical effect
is normally related to the dose administered. The antiinflammatory actions of corticosteroids are thought to involve
phospholipase A2 inhibitory proteins, collectively called lipocortins. Lipocortins, in turn, control the biosynthesis of
potent mediators of inflammation such as prostaglandins and leukotrienes by inhibiting the release of the precursor
molecule arachidonic acid. Likewise, the numerous adverse effectsrelated to corticosteroid use are usually related to
the dose administered and the duration of therapy.
Prednisone is the most commonly-prescribed oral corticosteroid. The drug is metabolized in the liver to its active
form, prednisolone. Relative to hydrocortisone, prednisone is roughly 4 times as potent as a glucocorticoid.
Prednisone is intermediate between hydrocortisone and dexamethasone in duration of action. Prednisone is used in
many conditions, including allograft rejection, asthma, systemic lupus erythematosus, and many other inflammatory
states. Prednisone has very little mineralocorticoid activity, so it is not used in the management of adrenal
insufficiency unless a more potent mineralocorticoid is administered concomitantly. Prednisone was first approved
by the FDA in 1955.
Rebamipide:
Effects:
OBJECTIVE: To investigate the effect of rebamipide (mucosta) on healing of gastric ulcer caused by various
etiologies.
MATERIAL AND METHOD: Thirty patients with gastric ulcer underwent gastric antral and body biopsies for
histopathology. Group classifications depended on H. pylori status using CLO test, histology or urea breath test and
history ofNSAIDs taking. All patients received rebamipide 100 mg, three times a day, for 8 weeks. The symptoms
and adverse effects were assessed in 4 weeks and 8 weeks after prescription. At the end of the present study, an
endoscopy was repeated to evaluate ulcer healing and biopsy for gastric inflammation grading.
RESULTS: According to the ulcer cause, there were seven patients with H. pylori+ NSAIDs+, nine patients with H.
pylori + NSAIDs-, three patients with H. pylori - NSAIDs +, and 11 patients with H. pylori - NSAIDs-. The ulcers
were completely healed in most patients with a history of NSAIDs use. There was a significant improvement of
symptom scores from baseline in all groups (5.9 vs. 0.6, p < 0.001). The improvement of gastric inflammation
scores were favorable in NSAIDs users (2.38 vs. 1.75, p = 0.011). All patients were satisfied as there were few
adverse effects.
CONCLUSION: Rebamipide is effective and well tolerated for treatment of gastric ulcers especially those caused by
NSAIDs, as it promotes the improvement of gastric inflammation scores, clinical symptoms, and ulcer healing.
Indication & Dosage
Oral
Peptic ulcer, Gastritis
Adult: 100 mg tid, in the morning, evening and before bed.
Contraindications
Lactation.
Special Precautions
Pregnancy, elderly and children.
Adverse Drug Reactions
Rash, pruritus, constipation, diarrhoea, nausea.
Mechanism of Action
Rebamipide is a mucosal protective agent and is postulated to increase gastric blood flow, prostaglandin
biosynthesis and decrease free oxygen radicals.
MIMS Class
Antacids, Antireflux Agents & Antiulcerants
Phillip Scheinberg, M.D., of the National Institutes of Health, Bethesda, Md., and
colleagues conducted a study to determine the effect of telomere attrition in acquired
severe aplastic anemia by measuring telomere length prior to immunosuppressive
therapy. The study included 183 patients with severe aplastic anemia who were treated
from 2000 to 2008. The pretreatment leukocyte (white blood cells involved in defending
the body against infectious disease) age-adjusted telomere length of patients with
severe aplastic anemia enrolled in immunosuppression protocols was analyzed for
correlation with clinical outcomes.
One hundred and four patients (57 percent) responded to immunosuppressive therapy.
The researchers found that there was no correlation between telomere length
(measured pretreatment) and the probability of response to the therapy. The response
rate for patients in the first quartile (shortest telomere lengths) was 56.5 percent; in the
second quartile, 54.3 percent; in the third quartile, 60 percent; and in the fourth quartile,
56.5 percent. Additional analysis demonstrated that telomere length was associated
with relapse, clonal evolution, and mortality. Telomere length was inversely correlated
with the probability of disease relapse. The probability of clonal evolution was higher in
patients in the first quartile (24.5 percent) than in quartiles 2 through 4 (8.4 percent).
"Survival between these 2 groups differed, with 66 percent surviving 6 years in the first
quartile compared with 83.8 percent in quartiles 2 through 4," the researchers write.
Reaction: