Furosemide 20 Mg Tablets
SUMMARY OF PRODUCT CHARACTERISTICS
1 NAME OF THE MEDICINAL PRODUCT
Furosemide 20mg Tablets
2. QUALITATIVE AND QUANTITATIVE COMPOSITION
Each tablet contains Furosemide 20mg
3 PHARMACEUTICAL FORM
Tablets.
White flat tablets with bevelled edge, 5mm diameter, embossed “F/20” on one face.
4. CLINICAL PARTICULARS
4.1. Therapeutic Indications
Management of :
Fluid retention.
Mild to moderate hypertension either alone or as an adjuvant.
4.2. Posology and Method of Administration
Adults:
The initial adult dose is 40mg daily, reduced to 20mg daily or 40mg on alternate days. In some patients daily doses of 80mg or higher (given in divided doses) may be required.
Children:
The usual daily dose is 1 to 3mg/kg body weight daily up to a maximum total dose of 40mg/day.
Elderly:
Dosage should be titrated until the required response is achieved because in the elderly Furosemide is generally eliminated more slowly.
For oral use.
4.3. Contra-indications
Furosemide is contraindicated in the presence of anuria, electrolyte deficiency, precoma associated with hepatic cirrhosis, hypersensitivity to Furosemide or sulphonamides.
4.4. Special Warnings and Special Precautions for Use
Use with caution in patients with impaired hepatic or renal function, diabetes mellitus or adrenal disease. It will be necessary to correct hypotension or hypovolaemia before commencing treatment. Regular monitoring of fluid and electrolyte balance is recommended. Use with care in elderly patients or those with prostatic hypertrophy or impairment of micturition. Latent diabetes may become manifest or insulin requirements of diabetic patients may increase.
4.5. Interactions with other Medicinal Product and other Forms of Interaction
Furosemide may enhance the toxicity of cardiac glycosides by depleting sodium -potassium concentrations. The action of antihypertensive agents such as methyldopa may be enhanced by Furosemide. Hypotension may occur if ACE inhibitors are added to Furosemide therapy. The dose of Furosemide should be reduced or the drug stopped before initiating the ACE inhibitor
The toxic effects of nephrotoxic antibiotics, particularly cefaloridine and the aminoglycoside antibiotics may be increased by Furosemide. The renal clearance of lithium is decreased by Furosemide, resulting in increased and possibly toxic serum levels. Concomitant administration should be avoided unless plasma levels can be monitored.
The action of diuretics such as Furosemide may be antagonised by certain nonsteroidal anti-inflammatory agents (e.g. indometacin, acetylsalicylic acid) and may cause renal failure in cases of pre-existing hypovolaemia.
Concurrent administration of glucocorticoids may cause sodium retention and exacerbate potassium loss. Furosemide decreases the effects of some drugs (e.g. antidiabetics and pressor amines) and may potentiate the effects of others (e.g. salicylates, theophylline, and curare-type muscle relaxants).
Interactions have also been reported with ototoxic antibiotics.
4.6. Pregnancy and Lactation
Furosemide should only be administered during pregnancy if considered essential by the physician and only for short-term therapy.
As it may inhibit lactation, or pass into the milk, Furosemide should be used with caution in nursing mothers.
4.7. Effects on Ability to Drive and Use Machines
Reduced mental alertness and rarely dizziness and blurred vision have been reported. Patients so affected should not drive or operate machines.
4.8. Undesirable Effects
Furosemide is generally well tolerated.
Eosinophilia is rare.
Bone marrow depression leading to blood dyscrasias, has been reported as a rare complication and necessitates withdrawal of treatment.
Occasionally, thrombocytopenia may occur. In rare cases, leucopenia and, in isolated cases, agranulocytosis, aplastic anaemia or haemolytic anaemia may develop.
Rarely, paraesthesiae may occur.
Hepatic encephalopathy in patients with hepatocellular insufficiency may occur (see Section 4.3).
Serum calcium levels may be reduced; in very rare cases tetany has been observed. Nephrocalcinosis / Nephrolithiasis has been reported in premature infants. Bone demineralisation and nephrocalcinosis have also been reported in adults, generally after long-term therapy.
Serum cholesterol and triglyceride levels may rise during furosemide treatment. During long term therapy they will usually return to normal within six months.
Glucose tolerance may decrease with furosemide. In patients with diabetes mellitus this may lead to a deterioration of metabolic control; latent diabetes mellitus may become manifest.
Hearing disorders and tinnitus, although usually transitory, may occur in rare cases, particularly in patients with renal failure, hypoproteinaemia (e.g. in nephritic syndrome).
Furosemide may cause a reduction in blood pressure which, if pronounced may cause signs and symptoms such as impairment of concentration and reactions, lightheadedness, sensations of pressure in the head, headache, dizziness, drowsiness, weakness, disorders of vision, dry mouth, orthostatic intolerance.
In isolated cases, intrahepatic cholestasis, an increase in liver transaminases or acute pancreatitis may develop.
The incidence of allergic reactions, such as skin rashes, photosensitivity, vasculitis, fever, interstitial nephritis or shock is very low, but when these occur treatment should be withdrawn. Skin and mucous membrane reactions may occasionally occur, e.g. itching, urticaria, other rashes or bullous lesions, erythema multiforme, bullous pemphigoid, exfoliative dermatitis, purpura.
As with other diuretics, electrolytes and water balance may be disturbed as a result of diuresis after prolonged therapy. Furosemide leads to increased excretion of sodium and chloride and consequently water. In addition excretion of other electrolytes (in particular potassium, calcium and magnesium) is increased. Symptomatic electrolyte disturbances and metabolic alkalosis may develop in the form of a gradually increasing electrolyte deficit or, e.g. where higher furosemide doses are administered to patients with normal renal function, acute severe electrolyte losses. Warning signs of electrolyte disturbances include increased thirst, headache, hypotension, confusion, muscle cramps, tetany, muscle weakness, disorders of cardiac rhythm and gastrointestinal symptoms. Pre-existing metabolic alkalosis (e.g. in decompensated cirrhosis of the liver) may be aggravated by furosemide treatment.
The diuretic action of furosemide may lead to or contribute to hypovolaemia and dehydration, especially in elderly patients. Severe fluid depletion may lead to haemoconcentration with a tendency for thromboses to develop.
Increased production of urine may provoke or aggravate complaints in patients with an obstruction of urinary outflow. Thus, acute retention of urine with possible secondary complications may occur, for example, in patients with bladder-emptying disorders, prostatic hyperplasia or narrowing of the urethra.
Severe anaphylactic or anaphylactoid reactions (e.g. with shock) occur rarely.
Side-effects of a minor nature such as nausea, malaise or gastric upset (vomiting or diarrhoea) may occur but are not usually severe enough to necessitate withdrawal of treatment.
As with other diuretics, treatment with furosemide may lead to transitory increases in blood creatinine and urea levels. Serum levels of uric acid may increase and attacks of gout may occur. Acute renal failure has been reported.
4.9. Overdose
In case of overdose there is a danger of dehydration and electrolyte depletion due to excessive diuresis. Therefore, the treatment of overdosage should be directed to correcting the dehydration and electrolyte imbalance. Gastric lavage may be useful if the ingestion is recent.
5.1. Pharmacodynamic Properties
Furosemide is a potent diuretic with rapid action. Its primary site of action is the ascending loop of Henle where it inhibits electrolyte reabsorption, thus enhancing the excretion of water, sodium, potassium and chloride ions.
5.2. Pharmacokinetic Properties
Furosemide is rapidly absorbed from the gastrointestinal tract. Bioavailability has been reported to be about 60-70%. It has a biphasic half-life in plasma with a terminal elimination phase up to about 2 hours but this is prolonged in neonates and in patients with hepatic and renal insufficiency. About 99% is bound to plasma proteins. It is excreted mainly in the urine, largely unchanged. Furosemide crosses the placental barrier and is excreted in milk. Clearance of Furosemide is not increased by haemodialysis.
5.3. Preclinical Safety Data
There is no preclinical data of relevance to the prescriber which are additional to that in other sections of the SPC.
6 PHARMACEUTICAL PARTICULARS
6.1 List of excipients
Lactose Starch (Maize)
Magnesium stearate Povidone
Sodium starch glycollate
6.2. Incompatibilities
None applicable.
Shelf Life
6.3.
36 months
6.4. Special Precautions for Storage
Do not store above 25°C. Keep the container tightly closed. Store in the original container.
6.5. Nature and Contents of Container
Securitainer: 100, 250, 500 and 1000 tablets Tampertainer: 100, 250, 500 and 1000 tablets PVC/Aluminium blister: 28 tablets
The securitainers and tampertainers are made of high density polypropylene material with low density polyethylene caps.
6.6. Instruction for Use/Handling Not applicable.
7 MARKETING AUTHORISATION HOLDER
Waymade PLC
Trading as Sovereign Medical
Sovereign House
Miles Gray Road
Basildon
Essex
SS14 3FR
United Kingdom
8 MARKETING AUTHORISATION NUMBER(S)
PL 06464/0206
9 DATE OF FIRST AUTHORISATION/RENEWAL OF THE AUTHORISATION
03/03/2006
10 DATE OF REVISION OF THE TEXT
17/12/2008