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Nsaids how safe are they
1.
Indian Journal of
Dental Sciences. www.ijds.in September 2012 Issue:3, Vol.:4 All rights are reserved Review Article Indian Journal of Dental Sciences E ISSN NO. 2231-2293 P ISSN NO. 0976-4003 1 Kavita Mittal NSAIDs - HOW SAFE ARE THEY 2 Sudhir Mittal 3 Anil Sharma 1 Prof & Head, Dept Of Pedodontics Abstract Desh Bhagat Dental College & Hospital, Muktsar This article analyses the drugs used to treat the symptoms and signs of inflammation. Most currently 2 Prof & Head, Dept Of Pedodontics available nonsteroidal anti -inflammatory drugs inhibit both cyclooxygenase -1 ( cox -1 ; constitutive Bhojia Dental College, Baddi 3 ) and cyclooxygenase -2 (cox-2 ; induced in settings of inflammation) activities , and thereby Prof & Head, Dept Of Orthodontics synthesis of prostaglandins and thromboxane. The inhibition of cox-2 is thought to mediate , at least College Of Dental Sciences, Bhavnagar, Gujrat in part , the antipyretic , analgesic and anti-inflammatory action of NSAIDs , but the simultaneous Address For Correspondence: inhibition of cox-1 results in unwanted side effects, particularly those leading to gastric ulcers , that Dr. Kavita Mittal result from decreased prostaglandin formation. The potential therapeutic advantage of selective Prof & Head cox-2 inhibitors is discussed. Dept Of Pedodontics Desh Bhagat Dental College & Hospital, Muktsar Email - care@jalandhardentalcare.com Key Words th NSAIDs- mechanism of action, selective cox-2 inhibitors, side effects of cox-1 inhibition, choice of Submission : 04 December 2011 NSAIDs th Accepted : 15 June 2012 Quick Response Code Pain, irrespective of the cause, is most Since NSAIDs find place in every common reason for which patient seeks prescription , it is must to understand , in dental treatment. Dentist must be able to addition to therapeutic benefits , the diagnose the cause and have a strategy for safety of NSAIDs. its management. Successful management of pain includes NSAIDs -accurate diagnose of the condition The anti-inflammatory, analgesic and -and appropriate dental treatment. antipyretic drugs are a heterogenous In the body , PGs , TXs ( thromboxane) group of compounds often chemically and LTs ( leukoterines ) are collectively Appropriate dental treatment removes unrelated which non theless share certain called eicosanoids. Eicosanoids are most the condition causing pain and usually therapeutic actions and side effects. They universally distributed autocoids in the provides rapid resolution of the are frequently called NSAIDs. To body. Practically every cell and tissue is symptoms. In addition to the above , understand the unwanted side effects , in capable of synthesizing one or more supportive drug therapy is given as an addition to therapeutic effect as anti- types of PGs and LTs. There are no adjunct to relieve patient from pain. Of inflammatory , it is important to preformed stores of PGs and LTs. They many dental conditions like pulpitis , understand the process of inflammation. are synthesized locally at the rate gingivitis/periodontitis , pericoronitis , governed by the release of arachidonic periapical abscess , or post extraction etc. In brief, inflammation process involves a acid from membrane lipids in response to , pain is usually caused by inflammation series of events that can be elicited by appropriate stimuli. and infection. numerous stimuli ( e.g. infectious agents , Cyclooxygenase ( COX ) pathway ischemia , antigen-antibody reaction , generates eicosanoids ( PGs , TXs ,and In addition to antibiotics to cover the thermal or physical injury ). Each type of Prostacyline ) , while Lipooxyganase infection , anti-inflammatory (steroidal stimuli provokes a characteristic pattern pathways generates open chain or non-steroidal) are used widely to of response that represents a relatively compounds ( LTs ). manage the pain. Non-steroidal provides minor variation. All tissues have cox , can form PGG2 , excellent relief due to their anti- PGH2 which are unstable compounds. inflammatory and analgesic effect. At microscopic level , response is usually accompanied by familiar clinical signs of Steroids can also be used for pain erythema , edema , tenderness , and pain. TX- thromboxane , PGI - Prostacycline , management but their use should be very HPETE - hydroperoxy eicosatetraenoic selective and limited. Inflammatory response occurs in three acid , HETE - Hydroxy eicosatetraenoic phases acid , SRS-A - Slow reacting substance of NSAIDs are prescribed to every patient -acute transient phase anaphylaxis. coming for dental treatment with pain -delayed sub-acute phase and sometimes they are prescribed even , -chronic proliferative phase Cyclooxygenase ( COX ) when not required. ©Indian Journal of Dental Sciences. (September 2012 Issue:3, Vol.:4) All rights are reserved. 124
2.
diffusion of H+
ions in the gastric mucosa. Deficiency of PGs reduces mucus and HCO3- secretion , tends to enhance acid secretion and may promote mucosal ischemia. Thus NSAIDs enhance aggressive factors in the gastric mucosa and are ulcerogenic. Side effects may range from mild dyspepsia and heart burn to ulceration sometimes with fatal results. These side effects are produced by all NSAIDs to varying extents : relative gastric toxicity is a major consideration in the choice of NSAIDs. On Renal Functions Adverse effects on renal functions are Biosynthesis of protaglandins (PG) and leukotrienes (LT) well recognised with the use of non selective NSAIDs. Cox is known to exist in two forms - pathological status. Cox-1 and Cox -2 while both forms Role of PGs in Renal Functions catalyse the same reactions. Side Effects Of NSAIDs - PGE2 and PGI2 increase water , Na+ and A splice variant of Cox -1 ( designated as The principal basis for therapeutic action K+ excretion and have a diuretic effects COX -3 ) has been found in dog brain. of NSAIDs is the inhibition of - PGE2 have been shown to have a This iso-enzyme is inhibited by prostaglandin synthesis. Since different frusemide like inhibitory effect on Cl- paracetamol but its role in human is not PGs , as described earlier , are implicated reabsorption as well. known. in different physiological functions in the - they cause renal vasodilation and inhibit body , their inhibition by the NSAIDs tubular reabsorption. COX-1 is a constitutive enzyme in most will have some adverse effects. So in - PGE2 antagonises ADH action and this cells. Its activity is not changed once the addition to sharing many therapeutic adds to diuretic effect . cell is fully grown. activities , NSAIDs share several - TXA2 cause renal vasodilation. COX -2 on the other hand , normally unwanted side effects as described present in insignificant amounts , is PGI2 , PGE2 and PGD2 evoke release of inducible by cytokines , growth factors , On Gastric Mucosa rennin. and other stimuli during inflammatory Most common is the propensity to induce As a result , PGs appear to function as process. gastric or intestinal ulceration. Highly intra-renal regulator of blood flow as well It is believed that eicosanoids produced selective cox2 inhibitors lack the as tubular reabsorption in kidneys. by cox-1 participate in physiological ( propensity to induce gastric or intestinal Rennin release in response to house keeping ) functions such as gastric ulceration. Gastric damage is brought sympathetic stimulation and other mucosa , hemostasis and maintenance of about by two mechanisms- influences may be facilitated by Pgs. renal functions while those produced by Although local irritation by oral cox-2 leads to inflammation and other administered drug allows back diffusion Effcts of NSAIDs due to inhibition of pathological changes. of acid into gastric mucosa and induce synthesis of Pgs However , certain sites in the kidney and t i s s u e d a m a g e , p a r e n t e r a l NSAIDs have little effects on renal brain constitutively express cox-2 which administration can also cause damage function in normal condition but may play physiological role. and bleeding. becomes significant in patients with CHF , hypovolemia , hepatic cirrhosis, renal Cyclic eicosanoids produce a wide In gastric mucosa , gastric prostaglandins disease and in patients receiving diuretics variety of actions depending upon the (PGs ) especially PGI2 and PGE2 serve as or anti- hyrertensives. particular PGs , species on which tested , cytoprotective agents. These eicosanoids tissue , hormonal status and other factors. inhibits acid secretion by the stomach by Acute renal failure may be precipitated PGs differ in their potency to produce a - under these circumstances because of given action and different PGs -enhancing mucosal blood flow - COX-1 dependent impairment of renal sometimes have opposite effects. Even - promotes secretion of cytoprotective blood flow and reduction of g.f.r. can the same PG may have opposite effect mucus in the intestine worsen renal insufficiency. under different circumstances. Since , - juxtaglomerular COX-2 dependant Na+ virtually all cells and tissues are capable Inhibition of synthesis of cox 1 and water retention. of forming PGs , they have been mediated gastro protective PGs (PGE2 - ability to cause papillary necrosis on implicated as mediators or modulators of and PGI2) renders the stomach more habitual intake. a number of physiological processes and susceptible to damage by inducing back ©Indian Journal of Dental Sciences. (September 2012 Issue:3, Vol.:4) All rights are reserved. 125
3.
FDA CATEGORY FOR
DRUG USE IN PREGENCY NSAIDs promotes salt and water CATEGORY Interpretation retention by reducing the PGs induced A Adequate, well-controlled studies in pregnant women have not shown an increased risk of fetal abnormalities to the fetus in any trimester of pregnancy. inhibition of both reabsorption of B Animal studies have revealed no evidence of harm to the fetus, however, there are no adequate and well-controlled studies in pregnant women. OR chloride and action of ADH. This may Animal studies have shown an adverse effect, but adequate and well-controlled studies in pregnant women have failed to demonstrate a risk to the cause edema in some patients treated with NSAIDs. Neuropathy is fetus in any trimester. uncommonly associated with long term C Animal studies have shown an adverse effect and there are no adequate and well-controlled studies in pregnant women. OR No animal studies have use of individual NSAIDs. been conducted and there are no adequate and well-controlled studies in pregnant women. D Adequate well-controlled or observational studies in pregnant women have demonstrated a risk to the fetus. However, the benefits of therapy may Impairment Of Platelet Functions outweigh the potential risk. For example, the drug may be acceptable if needed in a life-threatening situation or serious disease for which safer drugs COX-1 generated TXA2 - is a potent cannot be used or are ineffective. aggregating agent , and PGI2 - produced X Adequate well-controlled or observational studies in animals or pregnant women have demonstrated positive evidence of fetal abnormalities or risks. by vascular endotheliumis is an anti- The use of the product is contraindicated in women who are or may become pregnant. aggregating prostanoids. TXA2 produced by platelets and PGI2 produced by vascular endothelium probably constitutes a mutually ANALGESIC USE IN PREGNANCY OR LACTATION antagonistic system preventing Drugs FDA category for drug use in pregnancy May be used during pregnancy May Be Used While Breast Feeding aggregation of platelets in circulation and Acetaminophen B Yes Yes inducing aggregation on injury , when ASA C/Db Do not use in third trimester Caution plugging and thrombosis are needed. Diclofenac C/D Do not use in third trimester Caution NSAIDs inhibits the synthesis of both Flurbiprofen B/D Do not use in third trimester Yes TXA2 and PGI2 , but effects on platelets Ibuprofen B/D Do not use in third trimester Yes TXA2 (cox-1 generated aggregating Ketorolac B/D Do not use in third trimester Yes agent ) predominates. This accounts for the ability of these Ketoprofen B/D Do not use in third trimester Yes drugs to increase the bleeding time. Naproxen B/D Do not use in third trimester Yes Aspirin particularly have irreversible Codeine C Low dose, short duration is acceptable Yes effect on cox activity , effect lasting for Oxycodone B Low dose, short duration is acceptable Yes more than three days and require new Hydromorphone B Low dose, short duration is acceptable Yes platelet productions for the restoration of Mepridine B Low dose, short duration is acceptable caution enzyme activity. Pentazocine B Low dose, short duration is acceptable caution This side effect has been exploited in the prophylactic treatment of thromb oembolic disorders. Acute administration of 400-800mg of selective cox-2 inhibitor (celecoxib) in human beings has been found to suppress PGI2 production by about 80% , without inhibiting cox-1 generated TXA2 production and platelet aggregation. This suggests that cox-2 is a major source of PGI2 production in vivo. Since an important action of PGI2 is thought to be suppression of platelet activation , alteration of TXA2/PGI2 ratio that accompanies selective inhibition of cox2 is theoretically prothrombotic. Clinical muscles. relevance of this finding remains to be LTC4 and LTD4 are broncho constrictor in Other Side Effects determined but can be considered when many species including humans. - Intolerance choosing an NSAIDs for the treatment of Asthma may be induced due to imbalance Certain individuals display intolerance to patients particularly prone to thrombotic between dilators PGs and constrictors aspirin and most NSAIDs. This is events. Lts. In few individuals , aspirin like drugs manifest by symptoms that range from including cox 1 inhibitors , consistently vasomotor rhinitis with profuse watery On Broncheal Muscles induce asthma possibly by diverting secretion , angioneurotic edema , In general , PGFs and PGD2 contracts and arachidonic acid to produce excess LTs. generalized urticaria , and bronchial PGE2 relax bronchial and tracheal This sensitivity is not shared by selective asthma to laryngeal edema and broncho muscles. cox-2 inhibitors indicating that constriction , flushing , hypotension , and PGE2 and PGI2 produce broncho-dilation. suppression of cox-1 at the pulmonary shock. These reactions are not limited to TXA2 constricts human bronchial smooth site is responsible for the reaction. aspirin. An individual who exhibits ©Indian Journal of Dental Sciences. (September 2012 Issue:3, Vol.:4) All rights are reserved. 126
4.
intolerance to aspirin
will also react when If acetaminophen is insufficient , opioids themselves in producing different side given any of other NSAIDs , despite their are considered acceptable during effects and there are large inter- chemical diversity , thereby ruling out pregnancy provided they are given for a individual variation. No single drug is immunological basis for this reaction. short duration . Chronic opioid use can superior to others for every patient. Inhibition of COX with consequent result in fetal dependence, premature Choice of the drug is inescapably diversion of arachidonic acid to LTs may delivery & growth retardation. As with empirical. be involved , but there is no proof. pregnancy, acetaminophen is the analgesic of choice in lactation. ASA and The cause and nature of pain (mild , -Prolongation of gestation by NSAIDs diclofenac may increase bleeding and moderate or severe ; acute or chronic ; Synthesis of prostaglandins increases should be avoided if possible. Opioids ratio of pain ; inflammation) along with dramatically in the hours before are considered safe in lactation. consideration of risk factors in the given parturition. PGs are thus postulated to patient govern the selection of analgesic. have a major role in the initiation and Choice Of NSAIDs Also to be considered are past experience progression of labour and delivery. So , Vast majority of NSAIDs are organic of the patient, acceptability and inhibition of synthesis of PGs can delay acids and act as reversible competitive individual preference. Patients differ in and retard labour. However, labour can inhibitors of cyclooxygenase activity. their analgesic response to different occur in the absence of Pgs. However , these drugs do not inhibit the NSAIDs. If one NSAIDs is Accordingly some NSAIDs have been metabolism of arachidonate by unsatisfactory in a patient , it does not used as tacolytic agents to inhibit pre lipooxygenase. In fact , inhibition of mean that other will also be term labour. COX theoretically could lead to unsatisfactory. Some subjects feel better increased formation of leukotrienes by on a particular drug , but not on a closely -NSAIDs in pregnancy and lactation increasing the amount of arachidonate related ones. It is in this context that The use of analgesics during pregnancy that is available to lipooxygenase. availability of such a wide range of has been recently reviewed , and the NSAIDs may be welcomed. findings are summarized in the Table 1. Cox 1 and Cox 2 differ in their sensitivity to inhibition by certain anti- Optimal management of dental pain inflammatory drugs. This observation References during pregnancy is removal of the has led to the recent development of 1. GOODMAN & GILLMAN'S - The source of pain using local anesthesia. If , clinically useful agents that selectively pharmacological basis of however , post operative pain is present , inhibit Cox-2. These drugs show distinct Therapeutics-Tenth Edition an analgesic may be necessary and therapeutic advantages over non 2. ROBBINS - Pathological basis of s h o u l d b e m a d e a v a i l a b l e . selective NSAIDs agents , since COX- 2 Diseases -Sixth Edition Acetaminophen is clearly the analgesic is predominant cyclooxygenase at the site 3. K.D TRIPATHI - Essentials of of choice in all stages of pregnancy. The of inflammation but not at sites such as Medical Pharmacology - Sixth use of NSAIDs , including ASA , is less gastrointestinal tract. Thus, cox2 edition favourable , particularly late in inhibitors are anti-inflammatory but do 4. UPDENT April - June 2009 ; Vol : 8 , pregnancy. NSAIDs may predispose to not possess many of the adverse side Number 1 ineffective contractions during labour , effects of non selective cyclooxygenase increased bleeding during delivery or inhibitors. premature closure of ductus arteriosus of the heart. NSAIDs are therefore NSAIDs have their spectrum of adverse contraindicated in the third trimester . effects. They differ quantitatively among Source of Support : Nill, Conflict of Interest : None declared ©Indian Journal of Dental Sciences. (September 2012 Issue:3, Vol.:4) All rights are reserved. 127
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