Source: Pharmaceutical Benefits Scheme (AU) Revision Year: 2020 Publisher: Pfizer Australia Pty Ltd, Level 17, 151 Clarence Street, Sydney NSW 2000, Toll Free Number: 1800 675 229, www.pfizer.com.au
MINIDIAB is contraindicated in patients with:
MINIDIAB is also contraindicated in children.
The risks of hypoglycaemia, its symptoms and treatment, and conditions that predispose to its development should be explained to patients and responsible family members. Primary and secondary failure should also be explained. Patients should be informed of the potential risks and advantages of MINIDIAB and of alternative modes of therapy. They should also be informed about the importance of adhering to dietary instructions, of a regular exercise program, and of regular testing of urine and/or blood glucose.
Since glipizide belongs to the class of sulfonylurea agents, caution should be used in patients with G6PD-deficiency. Treatment of patients with G6PD-deficiency with sulfonylurea agents can lead to haemolytic anaemia and a non-sulfonylurea alternative should be considered.
All sulphonylurea agents are capable of producing severe hypoglycaemia. Proper patient selection, dosage, and instruction are important to avoid hypoglycaemic episodes. Renal or hepatic insufficiency may cause elevated blood levels of MINIDIAB and may also diminish gluconeogenic capacity, both of which increase the risk of serious hypoglycaemic reactions. Elderly, debilitated or malnourished patients and those with adrenal or pituitary insufficiency are particularly susceptible to the hypoglycaemic action of glucose-lowering drugs. Hypoglycaemia may be difficult to recognise in the elderly and in people who are taking betaadrenergic blocking drugs. Hypoglycaemia is more likely to occur when caloric intake is deficient, after severe or prolonged exercise, alcohol is ingested, or when more than one glucose-lowering drug is used.
When a patient stabilised on any diabetic regimen is exposed to stress such as fever, trauma, infection, or surgery, a loss of control may occur. At such times, it may be necessary to discontinue MINIDIAB and administer insulin.
The effectiveness of any oral hypoglycaemic drug, including MINIDIAB, in lowering blood glucose to a desired level decreases in many patients over a period of time, which may be due to progression of the severity of the diabetes or due to diminished responsiveness to the drug. The phenomenon is known as secondary failure, to distinguish it from primary failure in which the drug is ineffective in an individual patient when first given.
The metabolism and excretion of MINIDIAB may be slowed in patients with impaired renal and/or hepatic function. If hypoglycaemia should occur in such patients, it may be prolonged and appropriate management should be instituted.
In elderly patients, the initial and maintenance dosing should be conservative to avoid hypoglycaemic reactions
See section 4.4 Special warnings and precautions, Hypoglycaemia and section 4.2 Dose and method of administration.
Not for use in children (see section 4.3 Contraindications).
Blood and urine glucose should be monitored periodically. Measurement of glycosylated haemoglobin and/or fructosamine levels may be useful.
The pattern of laboratory test abnormalities observed with MINIDIAB was similar to that for other sulphonylureas. Occasional mild to moderate elevations of SGOT, LDH, alkaline phosphatase, BUN and creatinine were noted. One case of jaundice was reported. The relationship of these abnormalities to MINIDIAB is uncertain, and they have rarely been associated with clinical symptoms.
The hypoglycaemic action of sulphonylureas may be potentiated by certain drugs including nonsteroidal anti-inflammatory agents, quinolone antibiotics, and drugs that are highly protein bound, salicylates, sulphonamides, clofibrate, biguanides, diazoxide, chloramphenicol, probenecid, coumarins, monoamine oxidase inhibitors, and beta-adrenergic blocking agents.
Fluconazole: There have been reports of hypoglycaemia following the co-administration of glipizide and fluconazole, possibly the result ovorixf an increased half-life of glipizide.
Alcohol: Alcohol may increase the hypoglycaemic effect of MINIDIAB, which could lead to hypoglycaemic coma.
Angiotensin-converting Enzyme Inhibitors: The use of angiotensin converting enzyme inhibitors may lead to an increased hypoglycaemic effect in diabetic patients treated with sulphonylureas, including MINIDIAB. Therefore, a reduction in MINIDIAB dosage may be required.
H2 Receptor Antagonists: The use of H2 receptor antagonists (i.e. cimetidine) may potentiate the hypoglycaemic effects of sulphonylureas, including MINIDIAB.
Voriconazole: Although not studied, voriconazole may increase plasma level of sulfonylureas (e.g. tolbutamide, glipizide and glyburide) and therefore cause hypoglycaemia. Careful monitoring of blood glucose is recommended during co-administration.
When such drugs are administered to a patient receiving MINIDIAB, the patient should be observed closely for hypoglycaemia. When such drugs are withdrawn from a patient receiving MINIDIAB, the patient should be observed closely for loss of control. In vitro binding studies with human serum proteins indicated that MINIDIAB binds differently than tolbutamide and does not interact with salicylate or dicoumarol. However, caution must be exercised in extrapolating these findings to the clinical situation and in the use of MINIDIAB with these drugs.
Certain drugs tend to produce hyperglycaemia and may lead to loss of control. These drugs include the thiazides and other diuretics, corticosteroids, phenothiazines, thyroid products, oestrogens, progestogens, oral contraceptives, phenytoin, nicotinic acid, sympathomimetics, calcium channel blocking drugs, alcohol (chronic abuse), glucagon, and isoniazid. When such drugs are administered to a patient receiving MINIDIAB, the patient should be closely observed for loss of control. When such drugs are administered to (or withdrawn from) a patient receiving MINIDIAB, the patient should be observed closely for hypoglycaemia.
A potential interaction between oral miconazole and oral hypoglycaemic agents leading to severe hypoglycaemia has been reported. Whether this interaction also occurs with the intravenous, topical or vaginal preparations of miconazole is not known.
The risk of increase of effect of barbiturates is extremely low for pharmacokinetic reasons (non-ionic protein binding).
Tetracycline may interfere with determination of urine glucose. Cyclophosphamide and derivatives should also be used with care in diabetic patients since increased and decreased effects of sulphonylureas have been reported.
No data available.
Pregnancy Category C.
MINIDIAB (glipizide) was found to be mildly fetotoxic in rat reproductive studies at all dose levels (5-50 mg/kg). The fetotoxicity has been similarly noted with other sulphonylureas, such as tolbutamide and tolazamide. The effect is perinatal and believed to be directly related to the pharmacologic (hypoglycaemic) action of MINIDIAB. In studies in rats and rabbits no teratogenic effects were found. There are no adequate and well controlled studies in pregnant women.
Sulphonylureas are not suitable for the treatment of diabetes mellitus during pregnancy as significant metabolic changes occur during this period, which make control difficult.
Although it is not known whether MINIDIAB is excreted in human milk, some sulphonylurea drugs are known to be excreted in human milk. Because the potential for hypoglycaemia in nursing infants may exist, a decision should be made whether to discontinue nursing or to discontinue the drug, taking into account the importance of the drug to the mother. If the drug is discontinued and diet alone is inadequate for controlling blood glucose, insulin therapy should be considered.
The treatment of diabetes with MINIDIAB requires regular check-ups. Until optimum stabilisation has been achieved, for example during the change-over from other medications or during irregular use, the ability to drive and use machines may be impaired.
In controlled studies, the frequency of serious adverse reactions reported was low. Of 702 patients, 11.8% reported adverse reactions and in only 1.5% was MINIDIAB discontinued.
Hypoglycaemia: See section 4.4 Special warnings and precautions for use and section 4.8 Overdose.
Gastrointestinal: Gastrointestinal disturbances are the most common reactions. Gastrointestinal complaints were reported with the following approximate incidence: nausea and diarrhoea, (1.4%); constipation and gastralgia, (1%), vomiting (>1%). They appear to be dose-related and may disappear on division or reduction of dosage. Abdominal pain has also been reported. Cholestatic jaundice may occur rarely with sulphonylureas; MINIDIAB should be discontinued if this occurs.
Dermatologic: Allergic skin reactions including rash, erythema, morbilliform or maculopapular eruptions, urticaria, pruritus, and eczema have been reported in about one in seventy patients. These may be transient and may disappear despite continued use of MINIDIAB; if skin reactions persist, the drug should be discontinued. Porphyria cutanea tarda and photosensitivity reactions have been reported with sulphonylureas.
Metabolic: Hepatic porphyria and disulfiram-like reactions have been reported with sulphonylureas. In the mouse, MINIDIAB pretreatment did not cause an accumulation of acetaldehyde after ethanol administration. Clinical experience to date has shown that MINIDIAB has an extremely low incidence of disulfiram-like alcohol reactions.
Haematologic: Leucopoenia, agranulocytosis, thrombocytopenia, aplastic anaemia, haemolytic anaemia, and pancytopenia have been reported with sulphonylureas.
Endocrine reaction: Cases of hyponatraemia, and the syndrome of inappropriate antidiuretic hormone (SIADH) secretion have been reported with this and other sulphonylureas.
Miscellaneous: Dizziness, drowsiness, vertigo and headache have each been reported in about one in fifty patients treated with MINIDIAB. Confusion, tremor and malaise have also been reported. They are usually transient and seldom require discontinuance of therapy. These symptoms together with weakness, clouding of vision etc. may be signs of hypoglycaemia. However, the risk of severe or prolonged hypoglycaemia is low.
Eye Disorders: Visual disturbances such as blurred vision, diplopia, and abnormal vision including visual impairment and decreased vision, have each been reported in patients treated with MINIDIAB. They are usually transient and do not require discontinuance of therapy. However, they may also be symptoms of hypoglycaemia.
Hepatobiliary Disorders: Impaired hepatic function and hepatitis have been reported.
Reporting suspected adverse reactions after registration of the medicinal product is important. It allows continued monitoring of the benefit-risk balance of the medicinal product. Healthcare professionals are asked to report any suspected adverse reactions at www.tga.gov.au/reportingproblems.
Incompatibilities were either not assessed or not identified as part of the registration of this medicine.
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