Aceclofenac

Acenac is a non-steroidal agent with antiinflammatory and analgesic properties. Its mode of action is largely based on inhibition of prostaglandin synthesis. Acenac is a potent inhibitor of the enzyme cyclooxygenase, which is involved in the production of prostaglandins. It also stimulates cartilage matrix (glycosaminoglycans) synthesis.

Dose :

ADULT - 200 MG DAILY IN TWO DEVIDED DOSES

Monograph :

Aceclofenac tablet Presentation Acenac : Each film-coated tablet contains Aceclofenac BP 100 mg. Description Acenac is a non-steroidal agent with antiinflammatory and analgesic properties. Its mode of action is largely based on inhibition of prostaglandin synthesis. Acenac is a potent inhibitor of the enzyme cyclooxygenase, which is involved in the production of prostaglandins. It also stimulates cartilage matrix (glycosaminoglycans) synthesis. Indications and Uses Acenac is indicated for the relief of pain and inflammation in both acute and chronic pain like osteoarthritis, rheumatoid arthritis, ankylosing spondylitis, dental pain, post-traumatic pain, low back pain, gynaecological pain etc. Dosage and Administration Adults: The maximum recommended dose is 200 mg daily, taken as two separate 100 mg doses, one tablet in the morning and one in the evening. Children: There is no clinical data on the use of aceclofenac in children. Elderly: The pharmacokinetics of aceclofenac are not altered in elderly patients, therefore it is not considered necessary to modify the dose and dose frequency. Renal insufficiency: There is no evidence that the dosage of aceclofenac needs to be modified in patients with mild renal impairment. Hepatic insufficiency: The dose of aceclofenac should be reduced in patients with hepatic impairment. An initial daily dose of 100 mg should be administered. Side effects Generally aceclofenac is well tolerated. The majority of side effects observed have been reversible and of a minor nature and include gastrointestinal disorders (dyspepsia, abdominal pain, nausea and diarrhoea) and occasional occurance of dizziness. Dermatological side effects including pruritus and rash. Abnormal hepatic enzyme levels and raised serum creatinine have occasionally been reported. Contraindications Aceclofenac is contraindicated in patients previously sensitive to aceclofenac or aspirin or other NSAIDs. It should not be administered to patients with active or suspected peptic ulcer or gastrointestinal bleeding and moderate to severe renal impairment. Precautions Aceclofenac should be administered with caution to patients with symptoms indicative of gastrointestinal disorders, with a history of peptic ulceration, ulcerative colitis, Crohn's disease, hepatic porphyria, and coagulation disorders. Patients suffering from severe hepatic impairment must be monitored. Use in pregnancy & lactation Pregnancy: There is no information on the use of aceclofenac during pregnancy. Aceclofenac should not be administered during pregnancy, unless there are compelling reasons for doing so. The lowest effective dose should be administered. Lactation: There is no information on the secretion of aceclofenac in breast milk. The use of aceclofenac should therefore be avoided during lactation unless the potential benefits to the mother outweigh the possible risks to the children. Drug interactions Lithium and Digoxin: Aceclofenac, like other NSAIDs, may increase plasma concentrations of lithium and digoxin. Diuretics: Aceclofenac, like other NSAIDs, may inhibit the activity of diuretics. Anticoagulants: Like other NSAIDs, Aceclofenac may enhance the activity of anticoagulants. Quinolones: Convulsion may occur due to an interaction between quinolones and NSAIDs. Other NSAIDs and steroids: Concomitant therapy with aspirin, other NSAIDs and steroids may increase the frequency of side effects. Overdosage There is no human data available on the consequences of aceclofenac overdosage. After overdosage, following therapeutic measures to be taken: absorption should be prevented as soon as possible by means of gastric lavage and treatment with activated charcoal. Supportive and symptomatic treatment should be given for complications. Commercial Pack Acenac : Each box contains 10 blister strips of 10 tablets. Aceclofenac has no specific interaction information. Aceclofenac belongs to NSAIDs and will have the following interactions of NSAIDs: Interactions do not generally apply to topical NSAIDs ACE Inhibitors Antagonism of hypotensive effect and increased risk of renal impairment Adrenergic Neurone Blockers Antagonism of hypotensive effect Alpha-blockers Antagonism of hypotensive effect Angiotensin-II Receptor Antagonists Antagonism of hypotensive effect and increased risk of renal impairment with NSAIDs Antidepressants, SSRI Increased risk of bleeding Aspirin (also Benorilate) Avoid concomitant administration (increased side-effects) Baclofen Possibly reduced excretion of baclofen (possibly increased risk of toxicity) Beta-blockers Antagonism of hypotensive effect Since systemic absorption may follow topical application of beta-blockers to the eye the possibility of interactions, in particular, with drugs such as verapamil should be borne in mind Calcium-channel Blockers Antagonism of hypotensive effect Cardiac Glycosides Possibly exacerbation of heart failure, reduced GFR, and increased plasma-cardiac glycoside concentrations Ciclosporin Increased risk of nephrotoxicity Clonidine Antagonism of hypotensive effect Clopidogrel Increased risk of bleeding Corticosteroids Increased risk of gastro-intestinal bleeding and ulceration Interactions do not generally apply to corticosteroids used for topical action (including inhalation) Coumarins Anticoagulant effect possibly enhanced Change in patient's clinical condition, particularly associated with liver disease, intercurrent illness, or drug administration, necessitates more frequent testing. Major changes in diet (especially involving salads and vegetables) and in alcohol consumption may also affect anticoagulant control Diazoxide Antagonism of hypotensive effect Diuretics Risk of nephrotoxicity of NSAIDs increased; antagonism of diuretic effect Diuretics, Potassium-sparing Possibly increased risk of hyperkalaemia Drospirenone Possible hyperkalaemia (monitor serum potassium during first cycle) Heparins Possibly increased risk of bleeding Hydralazine Antagonism of hypotensive effect Ketorolac Avoid concomitant use (increased risk of side-effects and haemorrhage) Lithium Probably reduced excretion of lithium (risk of toxicity) Methotrexate Excretion of methotrexate probably reduced (increased risk of toxicity) Methyldopa Antagonism of hypotensive effect Mifepristone Manufacturer of mifepristone recommends avoid NSAIDs on theoretical grounds Minoxidil Antagonism of hypotensive effect Moxonidine Antagonism of hypotensive effect Nitrates Antagonism of hypotensive effect Nitroprusside Antagonism of hypotensive effect NSAIDs Avoid concomitant use (increased side-effects) Interactions do not generally apply to topical NSAIDs NSAIDs Avoid concomitant use (increased side-effects) Interactions do not generally apply to topical NSAIDs Pentoxifylline (oxpentifylline) Possibly increased risk of bleeding Phenindione Possibly enhanced anticoagulant effect Change in patient's clinical condition particularly associated with liver disease, intercurrent illness, or drug administration, necessitates more frequent testing. Major changes in diet (especially involving salads and vegetables) and in alcohol consumption may also affect anticoagulant control Phenytoin Effect of phenytoin possibly enhanced Quinolones Possibly increased risk of convulsions Ritonavir Plasma concentration possibly increased by ritonavir Sulphonylureas Possibly enhanced effect of sulphonylureas Tacrolimus Possibly increased risk of nephrotoxicity Zidovudine Increased risk of haematological toxicity Increased risk of toxicity with nephrotoxic and myelosuppressive drugs - for further details consult product literature Aceclofenac belongs to Analgesics but Analgesics has no interactions information

Paracetamol

PARACETAMOL, A PARA-AMINOPHENOL DERIVATIVE, HAS ANALGESIC AND ANTIPYRETIC PROPERTIES AND WEAK ANTI-INFLAMMATORY ACTIVITY.

Dose:

THE USUAL ADULT DOSE :- 0.5 TO 1 GM EVERY 4-6 HOURS UP TO A MAXIMUM OF 4 GM DAILY. CHILDREN UNDER 3 YEARS :- 10 MG/KG/BODY WT., 3 MONTHS TO 1 YEAR:- 60-120 MG, 1 TO 5 YEARS:- 120-250 MG, 6 TO 12 YEARS :- 250-500 MG EVERY 4-6 HOURS. ( SEE LIT FOR DETAILS.)

Monograph :

Paracetamol A white odourless crystalline powder. Sparingly soluble in water, soluble I in 20 of boiling water. I in 10 of alcohol, and I in 15 of IN sodium hydroxide; very slightly soluble in dichloromethane and in ether. Store in airtight containers. Protect from light. Adverse Effects and Treatment Side-effects of paracetamol are rare and usually mild, although haematological reactions including thrombocytopenia. leucopenia, pancytopenia, neu- tropenia, and agranulocytosis have been reported. Skin rashes, and other hypersensitivity reactions oc- cur occasionally. Overdosage with paracetamol can result in severe liver damage and sometimes acute renal tubular necrosis. Prompt treatment with acetylcysteine or methionine is essential and is discussed under Over- dosage, below. Effects on the kidneys. It can produce nephropathy. Effects on the pancreas. A review of drug-induced pan- creatitis reported that pancreatitis associated with paraceta- mol had only occurred in patients taking more than recommended doses and even then it had been a rare reac- tion. Hypersensitivity. Reactions, characterised by urticaria, dyspnoea, and hypotension, have occurred following the ad- ministration of paracetamol to adults and children. An- gioedema has also been reported. Fixed drug eruptions. confirmed by rechallenge have been described. Overdosage. Acute overdosage with paracetamol. whether accidental or deliberate, is relatively common. The conse- quences can be extremely serious because of the narrow mar- gin between therapeutic and toxic doses. Ingestion of as little as 10 to 15 g of paracetamol by adults may cause severe hepa- tocellular necrosis and, less often, renal tubular necrosis. Early features of overdosage such as nausea and vomiting usually settle within 24 hours: other early symptoms may in- clude lethargy and sweating. Abdominal pain may be the first indication of liver damage, which is not usually apparent for 24 to 48 hours and sometimes may be delayed for up to 4 to 6 days after ingestion. Liver damage is generally at a maxi- mum 72 to 96 hours after ingestion. Hepatic failure, enceph- alopathy, coma. and death may result. Complications of hepatic failure, include acidosis, cerebral oedema, haemor- rhage, hypoglycaemia, hypotension, infection, and renal fail- ure. An increasing prothrombin time is a reliable indicator of deteriorating liver function and it is recommended by some that the prothrombin time should be measured regularly. Measurement of serum concentrations of aspartate ami- notransferase and alanine aminotransferase is also considered to be of value. Patients receiving enzyme-inducing drugs or those with a history of alcohol abuse are at special risk of hepatic damage, as may be patients suffering from malnutrition such as those with anorexia or AIDS. It has also been suggest- ed that fasting may predispose to hepatotoxicity. Acute renal failure with acute tubular necrosis may develop, even in the absence of severe liver damage. Other non-hepatic symptoms that have been reported following paracetamol overdosage include myocardial abnormalities and pancreati- tis. Toxicity following overdosage with paracetamol has been at- tributed to the production of a minor but highly reactive me- tabolite, N-acetyl-p-benzoquinoneimine (NABQI) by mixed function oxidase enzymes in the liver and kidney. The amount of NABQI produced after normal doses of paracetamol is usually completely detoxified by conjugation with glutath- ione and excreted as mercaptopurine and cysteine conjugates. However, following paracetamol overdosage, tissue stores of glutathione become depleted, allowing NABQI to accumulate and bind to sulfhydryl groups within hepatocytes causing cell damage. Substances capable of replenishing depleted stores of glutathione. such as acetylcysteine or methionine, are thus used as antidotes in paracetamol overdosage. Acetylcysteine may also be involved in the repair of damaged tissue. Treatment of paracetamol overdosage. The management of paracetamol overdosage as practised in the UK and US has been the subject of several reviews. Prompt treatment is essential, even when there are no obvious symptoms, and all patients should be admitted to hospital. Gastric lavage should be carried out especially if the overdose was taken within the previous 2 hours; full supportive meas- ures should also be instituted. Some centres give activated charcoal to reduce gastro-intestinal absorption, especially in cases of multiple drug overdosage. However, if acetylcysteine or methionine is to be administered by mouth the charcoal is best cleared from the stomach to prevent it reducing the ab- sorption of the antidote. In order to assess the risk of liver damage, the plasma-para- cetamol concentration should be determined as soon as possi- ble. but not within 4 hours of ingestion. to ensure that peak concentrations are recorded. The patient's plasma-paraceta- mol concentration is compared against a standard nomogram reference line on a plot of plasma-paracetamol concentration against hours after ingestion. A semi-logarithmic plot or a lin ear plot may be used. Generally, antidote treatment is required if the patient's plas ma-paracetamol concentration is higher than this line. Plas- ma-paracetamol measured more than 16 hours after ingestion are not reliable indicators of hepatic toxicity. Furthermore. the nomogram may not be suitable for use when patients have taken modified-release preparations of paracetamol. Some suggestions for modified strategies for the use of the Rumack-Matthew nomogram in the face of overdosage with modified-release preparations have been made. Antidote treatment should be started as soon as possible after suspected paracetamol ingestion and should not be delayed while awaiting the results of plasma assays. Once the results become available, treatment may be stopped if the initial concentration is below the nomogram reference line. However, if the initial concentration is above the reference line, the full course of antidote must be administered and should not be discontinued when subsequent plasma concentrations fall be- low the reference line. Patients receiving enzyme-inducing dnigs such as carbamazepine, phenytoin. phenobarbitone. ri- fampicin, or those with malnutrition or a history of alcohol abuse should receive an antidote if their plasma-paracetamol concentrations are up to 50% below the standard reference line. Choice of antidote. Acetylcysteine is usually the an- tidote of choice but there is some variance over the route of administration used. Although intravenous administration has been associated with anaphylactic reactions it is the preferred route in the UK because of concerns over the effects of vom- iting and activated charcoal on oral absorption. Nausea and vomiting are amongst the most common early symptoms of paracetamol overdosage and may be exacerbated by the ex- tremely disagreeable taste and odour of oral acetylcysteine. However, oral administration is the usual route of choice in the USA and experience there suggests that it is effective and that the outcome of treatment is not adversely affected by the use of activated charcoal. An alternative in the UK is methionine by mouth, which is cheaper and easier to administer than intravenous acetylcysteine. It may also be used in the UK in situations where a patient cannot be transferred to hospital provided it is given within 10 to 12 hours of the overdose. Methionine ab- sorption is impaired if activated charcoal has been adminis- tered or in patients who are vomiting. Acetylcysteine is most effective when administered during the first 8 hours following ingestion of the overdose and the effect diminishes progressively thereafter. It used to be believed that starting treatment more than 15 hours after overdosage was of no benefit and might possibly aggravate the risk of hepatic encephalopathy. However, late administration has now been shown to be safe and studies of patients treated up to 36 hours after ingestion suggest that beneficial results may be obtained up to and possibly beyond 24 hrs. Further- more, administration of intravenous acetylcystcine to patients who had already developed fulminant hepatic failure has been shown to reduce morbidity and mortality. In the UK. an initial dose of 150 mg per kg body-weight of acetylcysteine in 200 mL of glucose 5% is given intravenous- ly over 15 minutes, followed by an intravenous infusion of 50 mg per kg in 500 mL of glucose 5% over the next 4 hours and then 100 mg per kg in one litre over the next 16 hours. The volume of intravenous fluids should be modified for chil- dren. If an anaphylactoid reaction develops, the infusion should be stopped and an antihistamine administered; it may be possible to continue the acetylcysteine infusion at a slower rate. In the USA. acetylcysteine is given by mouth in an initial dose of 140 mg per kg as a 5% solution followed by 70 mg per kg every 4 hours for an additional 17 doses. Somet' have suggested using a larger loading dose of acetylcysteine when it is given orally with activated charcoal whereas others" have found that the efficacy of acetylcysteine is not adversely affected by prior administration of activated charcoal and consider that increasing the acetylcysteine dose appears to be unwarranted. Methionine is an alternative to acetylcysteine and, likewise, is most effective when given as early as possible following pa- racetamol overdosage. However, it is not as effective in late presentation and the incidence and severity of hepatic damage is greater if treatment with methionine is started more than 10 hours after ingestion; it may also precipitate hepatic encephalopathy. The usual dose of methionine is 2,5 g by mouth every 4 hours for 4 doses starting less than 10 to 12 hours after ingestion of the paracetamol. It has also been given intravenously. The lit- erature relating to the use of methionine in paracetamol poi- soning is. in general, imprecise as to the form of methionine used. In the UK. the doses quoted above refer to DL-methio- nine. Preparations containing both methionine and paraceta- mol (co-methiamol) have been formulated for use in situations where overdosage may occur. However, the issue of whether methionine should be routinely added to paracetamol preparations is contentious for medical and ethical reasons. Histamine H;-receptor antagonists. It has been suggested that since cimetidine blocks the hepatic cytochrome P450 mixed function oxidase system, it might be of use as an adjunct to acetylcysteine for patients whose production of the toxic mc- tabolite of paracetamol is increased due to enzyme induction. Although there have been several anecdotal reports claiming benefit for cimetidine in patients with paracetamol poisoning, there is no current evidence to support these claims. Liver transplantation may be considered as a last recourse in some patients. Precautions Paracetamol should be given with care to patients with impaired kidney or liver function. It should also be given with care to patients with alcohol depend- ence. Breast feeding. The amount of paracetamol distributed into breast milk is considered by some authorities to be too small to be harmful to a breast-fed infant. Pharmacokinetic studies in 12 nursing mothers given a single dose of paracetamol showed that peak paracetamol concentrations in breast milk of 10 to 15 ng per mL were achieved in 1 to 2 hours. Plasma concentrations were determined in 2 mothers: a breast milk/plasma ratio of about 1 was reported. Similar findings were reported from another study. Renal impairment. Caution is recommended when giving paracetamol to patients with renal impairment. Plasma con- centrations of paracetamol and its glucuronide and sulphate conjugates are increased in patients with moderate renal fail- ure and in patients on dialysis. It has been suggested that paracetamol itself may be regenerated from these metabo- lites. There are conflicting data on whether the conjugates of paracetamol accumulate in patients with renal impairment receiving multiple doses. Interactions The risk of paracetamol toxicity may be increased in patients receiving other potentially hepatotoxic drugs or drugs that induce liver microsomal en- zymes. The absorption of paracetamol may be ac- celerated by drugs such as metoclopramide. Excretion may be affected and plasma concentra- tions altered when administered with probenecid. Cholestyramine reduces the absorption of paraceta- mol if given within one hour of paracetamol admin- istration. Antibacterials. For the effects of paracetamol on chloram- phenicol. see chloramphenicol. Anticoagulants. For the effects of paracetamol on oral anti- coagulants, see under Warfarin. Antiepileptics. For the effects of paracetamol on lamotrigi- Ne, see lamotrigine. Antivirals. For reports of adverse effects of the liver associ- ated with concomitant use of paracetamol and antiviral drugs, see under Interferons and Zidovudine. Probenecid. Pretreatment with probenecid can decrease pa- racetamol clearance and increase its plasma half-life. Al- though urinary excretion of the sulphate and glucuronide conjugates of paracetamol are reduced, that of paracetamol is unchanged. Pharmacokinetics Paracetamol is readily absorbed from the gastro-in- testinal tract with peak plasma concentrations oc- curring about 10 to 60 minutes after oral administration. Paracetamol is distributed into most body tissues. It crosses the placenta and is present in breast milk. Plasma-protein binding is negligible at usual therapeutic concentrations but increases with increasing concentrations. The elimination half-life of paracetamol varies from about I to 3 hours. Paracetamol is metabolised predominantly in the liver and excreted in the urine mainly as the glucuro- nide and sulphate conjugates. Less than 5% is ex- creted as unchanged paracetamol. A minor hydroxylated metabolite (N-aceryl-p-benzoquinon- eirnine) which is usually produced in very small amounts by mixed-function oxidases in the liver and kidney and which is usually detoxified by conjuga- tion with glutathione may accumulate following pa- racetamol overdosage and cause tissue damage. Absorption. The absorption of paracetamol was slow and incomplete in vegetarian subjects compared with non-vege- tarian subjects. Uses and Administration Paracetamol, a para-aminophenol derivative, has an- algesic and antipyretic properties and weak anti-in- flammatory activity. Paracetamol is given by mouth or as a rectal suppository for mild to moderate pain and for fever. Paracetamol is often the analge- sic or antipyretic of choice especially in patients in whom salicylates or other NSAIDs are contra-indi- cated. Such patients include asthmatics or those with a history of peptic ulcer, or children in whom salicylates are contra-indicated because of the risk of Reye's syndrome. The usual adult dose by mouth is 0.5 to I g every 4 to 6 hours up to a maximum of 4 g daily. Usual dos- es in children are: under 3 months, 10 mg per kg body-weight (reduce to 5 mg per kg if jaundiced); 3 months to I year, 60 to 120 mg: I to 5 years, 120 to 250 mg-, 6 to 12 years, 250 to 500 mg. These doses may be given every 4 to 6 hours when necessary up to a maximum of 4 doses in 24 hours. For post-im- munisation pyrexia. a dose of 60 mg has been rec- ommended for children 2 to 3 months of age. A second dose may be given after four to six hours', if the pyrexia persists after that 'dose, the parent should seek medical advice. Rectal doses for adults and children over 12 years of age are 0.5 to I g. Rectal doses in younger children are: I to 5 years, 125 to 250 mg; 6 to 12 years, 250 to 500 mg. Doses may be administered up to 4 times daily. Headache. Non-opioid analgesics such as paracetamol. as- pirin. and other NSAIDs are often tried first for the sympto- matic treatment of various types of headache including migraine and tension-type headache . These drugs given at the onset of symptoms can successfully treat an acute attack of migraine. However, absorption may be poor due to gastric stasis which is commonly present in mi- graine. For this reason dispersible and effervescent prepara- tions and compound preparations containing drugs such as metoclopramide which relieve gastric stasis have been advo- cated. Pain. Paracetamol is used in the management of mild to mod- erate pain . It is of similar potency to aspirin, but with weak anti-inflammatory activity. Paracetamol may also be used as an adjunct to opioids in the management of severe pain such as cancer pain . Paracetamol is the preferred choice for pain in infants and children because of the association of aspirin with Reye's syndrome in this age group. In the treatment of rheumatic disorders, a weak anti-inflammatory effect limits the role of paracetamol. How- ever, it may be of benefit for simple pain control in rheuma- toid arthritis and ankylosing spondylitis although these patients usually require the additional anti-inflammatory effects provided by NSAIDs. Synovial inflammation is usually only a minor com- ponent of osteoarthritis . and paracetamol is generally recommended as first choice of treatment before NSAIDs arc tried. Paracetamol is useful for the relief of acute low back pain . Dependence and tolerance are not a problem with non-opioid analgesics such as paracetamol. but there is a ceiling of effi cacy, above which increasing the dose has no further thera- peutic effect. Paracetamol Suppositories 80 mg and 170 mg Composition Each suppository contains : Paracetamol 80 mg, Paracetamol 170 mg Suppository Base q.s. INDICATIONS: Symptomatic relief of pain and fever. CONTRAINDICATIONS:  Known allergy to paracetamol  Serious liver disorder  Rectal bleeding or inflammation (contraindication related directly to the administration route of the medicine) PRECAUTIONS AND WARNINGS: Intake of aspirin and paracetamol should not be alternated. Paracetamol should be given with care to patients with impaired liver or kidney function. In the event of uric acid or sugar content tests, the patient should be advised to disclose the intake of paracetamol. If the pain persists for more than 5 days or the fever for more than 3 days, or in the event of aggravation, treatment should not be continued without seeking advice from the doctor. Severe or recurrent pain or high or continued fever may be indicative of serious illness. ADVERSE REACTIONS: If used as directed, paracetamol rarely causes severe toxicity or side effects. In some rare cases a cutaneous eruption or an allergic reaction may occur. Redness of the mucous membrane of the rectum and minor local vascular changes may be reported. Hepatic necrosis may occur after overdosage. Reasons for Immediate discontinuation of the drug  Exceptional biological changes requiring a blood analysis  Abnormally low count of certain blood constituents(platelets)  Local effects related to administration route. These are all the more frequent and severe if the duration of treatment Is prolonged and the frequency of intake and the dosage are high. DRUG INTERACTIONS: The medicine contains paracetamol. It should not be combined with other paracetamol preparations so as not to exceed the recommended daily dose. Drugs which induce hepatic microsomal enzymes such as alcohol, rifampicin, barbiturates and other anti-convulsants may increase the hepatotoxicity of paracetamol particularly after overdosage. The therapeutic effects of paracetamol may also be decreased. DOSAGE AND ADMINISTRATION: The recommended usual daily dose depends on the weight of the infant. It is determined at 60 mg/kg/day, to be spaced out in 4 different intakes per day. For information only: 80 mg:- Up to 7 kg (about 6 months old): 1 suppository of 80 mg, to take twice if needed, after 6 hours, without taking more than 4 suppositories per day. 170 mg:- From 12-16 kg (about 2-4 years old): 1 suppository of 170 mg, to take twice if needed, after 6 hours, without taking more than 4 suppositories per day. The approximate ages as a function of body weight are given for example only. In case of any doubt, the doctor should be consulted for advice. The rectal route of administration should be adopted. Systemic intakes avoid prickling effects of fever. For infants, the intakes must be spaced out every 6 hours. In the event of serious kidney disorder (severe renal insufficiency), intakes should occur at intervals of 8 hours minimum. Do not exceed 3 days of treatment in the event of fever or 5 days of treatment in the event of pain without the advice of the doctor. OVERDOSAGE: In the event of overdosage or accidental ingestion of a very high dose, the doctor should be immediately consulted. ----------------------------------------------------------------------------------------------------------------

Serratiopeptidase

IT IMPROVES AGGRAVATED CIRCULATION IN THE INFLAMMATORY FOCUS BY BREAKING DOWN ABNORMAL EXUDATES AND PROTEIN AND BY PROMOTINIG THE ABSORPTION OF THE DECOMPOSED PRODUCTS THROUGH THE BLOOD AND LYMPHATIC VESSELS. IT ALSO ACELERATES THE ELIMINATION OF SPUTUM. PUS AND HAEMATOMA BY BREAKING DOWN THE LIQUIFYING MUCUS SECRETIONS AND FIBRIN CLOTS. ANOTHER MAJOR USEFUL ACTION BEING INCREASED CONCENTRATION OF ANTIBIOTICS IN THE FOCUS IN INFECTION.

Dose:

5-10 MG THRICE A DAY BEFORE MEALS, MAXIMUM 20 MG TDS

Monograph:

SERRATIOPEPTIDASE  is a protiolytic enzyme derivedfrom a species of bacteria called Seiratia. On oral .administration, it is absorbed unchanged into systemic circulation,from where it penetrates into all tissues.It reaches higher concentration in inflamed tissues. In ccontrast to chymo-trypsin. a fungal enzyme, Serratiopeptidase is a bacterial enzyme, hence, allergic reactions to it are relatively rarer It exerts a number of pioteolytic actions in the body to help in controlling the inflammatory process and augmenting the repair activity of the body: They can be summarised thus I Augmenting plasmin activity by inhibiting its inactivators in the plasma. This helps to restore the disturbed microcirculation. 2. Helps the body to break down pus and debris of dead microbes and damaged cells to eliminate unwanted material from the lesion. 3. Dissolves complex respiratory mucus/sputum strands into smaller molecules having lower viscosity, to enhance expectoration. 4 Breaks down complement to reduce humoral inflammatory processes. 5. Improvement in microcirculation results in enhanced penetration of all classes of antibiotics into inflamed sites. 6. Reduces engorgement of breast and reduces pain and swelling to reduce discomfort. 7. Having no relationship in chemical structure or activity to NSAIDs, it can be used in patients allergic or intolerant to the latter, whenever soft tissue anti- inflammatory activity is called for. 8. By breaking down pus, restoring microcirculation in capillaries and lymphatic, destroying complement and augmenting plasmin activity, it reduces Oedema of inflammatory origin, along with discomfort and pain due to it.