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The Use And Misuse Of Nonsteroidal Anti-inflammatory Drugs (nsaids)
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Hypersensitivity.
Two types of hypersensitivities experienced in NSAIDs use are Cutaneous Hypersensitivity and nonallergic anaphylaxis.The cutaneous pattern of NSAID-induced crossreactions includes cross-reacting urticaria and angioedema in patients with or without chronic idiopathic urticarial. The mechanisms are not completely understood, but in patients with CIU, COX-1 inhibition has beendemonstrated.
Nonallergic Anaphylaxis, Previously known as anaphylactoid or pseudoallergic reaction, it is observed in cross-reactive patients and presumably mediated by inhibition of COX-1(Mario, 2008)
Certain individuals display hypersensitivity to aspirin and NSAIDs, as manifested by symptoms that range from vasomotor rhinitis with profuse watery secretions, angioedema, generalized urticaria, and bronchial asthma to laryngeal edema, bronchoconstriction, flushing, hypotension, and shock. Aspirin intolerance is a contraindication to therapy with any other NSAID because cross-sensitivity can provoke a life-threatening reaction reminiscent of anaphylactic shock. Despite the resemblance to anaphylaxis, this reaction does not appear to be immunological in nature.
Although less common in children, this syndrome may occur in 10% to 25% of patients with asthma, nasal polyps, or chronic urticaria, and in 1% of apparently healthy individuals. It is provoked by even low doses (<80 mg) of aspirin and apparently involves COX inhibition. Cross-sensitivity extends to other salicylates, structurally dissimilar NSAIDs, and rarely acetaminophen (see below). Treatment of aspirin hypersensitivity is similar to that of other severe hypersensitivity reactions, with support of vital organ function and administration of epinephrine. Aspirin hypersensitivity is associated with an increase in biosynthesis of LTs, perhaps reflecting diversion of AA to lipoxygenase metabolism. Indeed, results in a small number of patients suggest that blockade of 5-lipoxygenase with the drug zileuton (no longer marketed in the United States) or use of the leukotriene receptor antagonists may ameliorate the symptoms and signs of aspirin intolerance, albeit incompletely.
Aspirin Resistance. All forms of treatment failure with aspirin have been collectively called "aspirin resistance." Although this has attracted much attention, there is little information concerning the prevalence of a stable, aspirin-specific resistance or the precise mechanisms that might convey this "resistance." Genetic variants of COX-1 that cosegregate with resistance have been described, but the relation to clinical outcome is not clear.
INTERACTIONS OF NSAIDS
Concomitant NSAIDs and Low-Dose Aspirin. Many patients combine either NSAIDs or COX-2 inhibitors with "cardioprotective" low-dose aspirin. Epidemiological studies suggest that this combination therapy increases significantly the likelihood of gastrointestinal adverse events over either class of NSAID alone.
Prior occupancy of the active site of platelet COX-1 by the commonly consumed tNSAID ibuprofen impedes access of aspirin to its target Ser 529 and prevents irreversible inhibition of platelet inhibition (Catella-Lawson et al., 2001). Epidemiological studies have provided conflicting data as to whether this adversely impacts clinical outcomes, but they generally are constrained by the use of prescription databases to examine an interaction between two drug groups commonly obtained without prescription. Evidence in support of this interaction has been observed in cEomparing ibuprofen-treated patients with and without aspirin in two coxib outcome studies (CLASS and TARGET), but the trials were not powered to address this question definitively. In theory, this interaction should not occur with selective COX-2 inhibitors, because mature human platelets lack COX-2.
Other Drug Interactions. Angiotensin-converting enzyme (ACE) inhibitors act, at least partly, by preventing the breakdown of kinins that stimulate prostaglandin production. Thus, it is logical that NSAIDs might attenuate the effectiveness of ACE inhibitors by blocking the production of vasodilator and natriuretic prostaglandins. Due to hyperkalemia, the combination of NSAIDs and ACE inhibitors also can produce marked bradycardia leading to syncope, especially in the elderly and in patients with hypertension, diabetes mellitus, or ischemic heart disease. NSAIDs may increase the frequency or severity of gastrointestinal ulceration when combined with corticosteroids and augment the risk of bleeding in patients receiving warfarin. Many NSAIDs are highly bound to plasma proteins and thus may displace other drugs from their binding sites. Such interactions can occur in patients given salicylates or other NSAIDs together with warfarin, sulfonylurea hypoglycemic agents, or methotrexate; the dosage of such agents may require adjustment to prevent toxicity. The problem with warfarin is accentuated, both because almost all NSAIDs suppress normal platelet function and because some NSAIDs also increase warfarin levels by interfering with its metabolism; thus, concurrent administration should be avoided.
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ABSRACT - [ Total Page(s): 1 ]ABSTRACT COMING SOON ... Continue reading---
CHAPTER TWO - [ Total Page(s): 3 ]EXCLUSION CRITERIAAll pharmacists not practicing as community pharmacistsAll patent medicine vendors and outlets2.4 SAMPLE SIZE DETERMINATIONa. Retrospective review of prescriptions: All prescriptions from November 2013 and April 2014 were obtained from the Outpatient Pharmacy Department prescription bank. The prescriptions containing NSAIDs were separated from those without NSAIDs.b. Ilorin metropolis is made up of three local government areas: Ilorin West, Ilori ... Continue reading---
CHAPTER THREE - [ Total Page(s): 8 ]CHAPTER THREE RESULTS3.1 RESULTS OF ANALYSIS OF PRESCRIPTIONS/TREATMENT SHEETSOut of 1497 prescription sheets 1297 prescriptions contained NSAIDs with total of 1392 NSAIDs. The prescribing rate was hence found to be 86.6%. 7.3% of prescriptions contained more than one NSAIDs. ... Continue reading---
CHAPTER FOUR - [ Total Page(s): 2 ]CHAPTER FOURDISCUSSIONStudy of the Prescribing pattern of Nonsteroidal Antiinflammatory Drugs indicated more number of females assess health care for pain and related conditions than their male counterpart (Table 3.1), although there is widespread assumption that women will consult more readily for all symptoms or conditions and that men will be more reluctant or will delay consulting may result in health care providers assuming that women have a lower level of symptom severity before deciding ... Continue reading---
CHAPTER FIVE - [ Total Page(s): 1 ]CHAPTER FIVE CONCLUSIONThe prescribing rate of NSAIDs was high. The prevalence of NSAIDs misuse by residents was high Ibuprofen was the most highly misused among the residents. Dispensing pattern of NSAIDs by Pharmacists appeared to agree with the choice of medication use among residents. Educational status, occupation, prior knowledge of medication use and dispensing pattern of Pharmacists are factors that can influence public choice of NSAIDs use. ... Continue reading---
REFRENCES - [ Total Page(s): 5 ]Slater DM, Zervou S, Thornton S. (2002). Prostaglandins and prostanoid receptors in human pregnancy and parturition. J. Soc. Gynecol. Investig. 9:118-124.Soleymani F, Ahmadizar A and Abdollahi MA(2013). Survey on the factors influencing the pattern of medicine's use: Concerns on irrational use of drugs. J Res Pharm Pract. 2(2), 59–63.Solomon SD, McMurray JJ, Pfeffer MA, Wittes J, Fowler R, Finn P, Anderson WF, Zauber A, Hawk E, Bertagnolli M (2005). Cardiovascular risk associated with c ... Continue reading---
