Source: Medicines & Healthcare Products Regulatory Agency (GB) Revision Year: 2019 Publisher: Generics [UK] Ltd. t/a Mylan, Station Close, Potters Bar, Herts EN6 1TL, U.K.
In patients with uncomplicated hypertension, symptomatic hypotension has been observed in rare cases after the first dose or after an increased dose. Marked activation of the renin-angiotensin- aldosterone system occurs under certain conditions, especially in the event of severe fluid and sodium depletion (low salt diet, prolonged diuretic treatment, dialysis, diarrhoea or vomiting), renal artery stenosis, heart failure and cirrhosis of the liver with oedema and/or ascites. The ACE inhibitor’s suppression of the renin-angiotensin-aldosterone system may cause severe arterial hypotension and/or functional renal insufficiency, especially at the first dosage, when the dose is increased and during the first two weeks of treatment. Severe hypotension may lead to fainting and/or ischaemic lesions in organs with arterial disorders (e.g. acute myocardial infarction, cerebrovascular infarction).
In such risk patients, including those with angina pectoris, ischaemic heart disease or cerebrovascular disorders, trandolapril treatment should be initiated under close medical supervision in low doses, with careful dose adjustment. In the event of prior diuretic treatment, in some patients particularly if this treatment has been recently instituted, the fall in blood pressure on initiation of treatment with trandolapril may be excessive. It is recommended to discontinue the diuretic treatment at least 72 hours before the trandolapril treatment is initiated and begin with 0.5 mg daily (see section 4.5).
Fluid and salt depletion should be remedied before initiating trandolapril treatment.
If the patient develops arterial hypotension or renal insufficiency during treatment, dose reduction or suspension of the treatment with trandolapril and/or diuretics may be necessary.
A case of arterial hypotension occurring after the initial dose does not exclude subsequent treatment with trandolapril provided the dose is adjusted carefully.
If symptomatic hypotension occurs, the patient should be placed in a supine position and, if necessary, receive an intravenous infusion of physiological saline. Intravenous atropine may be necessary if there is associated bradycardia.
Treatment of renovascular hypertension is carried out by revascularisation.
However, ACE inhibitors may be of use until revascularisation can be effected, or if such a procedure is not to be carried out. The risk of severe arterial hypotension and renal insufficiency is increased when patients with prior unilateral or bilateral renal artery stenosis are treated with an ACE inhibitor. Diuretics may further increase the risk. Loss of renal function may occur with only small changes in the serum creatinine, even in patients with unilateral renal artery stenosis. For these patients treatment should be initiated in the hospital under close medical supervision with low doses and careful dose adjustment. Diuretic treatment should be discontinued, and renal function and serum potassium monitored during the early weeks of treatment.
Evaluation of the patient should include assessment of renal function prior to initiation of therapy and during treatment. Proteinuria may occur if renal impairment is present prior to therapy or relatively high doses are used.
In the event of renal insufficiency the dose must be reduced if the creatinine clearance is ≤0.5 ml/s (≤30 ml/min) (see section 4.2). In patients with renal insufficiency it is recommended that renal function and serum potassium be monitored closely during the early weeks of treatment and subsequently as appropriate. Some hypertensive patients without previously diagnosed renal disease may develop increases in serum urea nitrogen and serum creatinine when trandolapril is given concurrently with diuretics. Proteinuria may occur.
In patients with renal insufficiency, congestive heart failure or unilateral or bilateral renal artery stenosis, in the single kidney as well as after renal transplantation, there is a risk of impairment of renal function. If recognised early, such impairment of renal function is reversible upon discontinuation of therapy.
Additionally, in patients with renal insufficiency, the risk of hyperkalaemia should be considered and the patient’s electrolyte status checked regularly.
There is no experience regarding the administration of trandolapril in patients with a recent kidney transplantation. Treatment with trandolapril is therefore not recommended.
As trandolapril is a prodrug metabolised to its active form in the liver, particular caution and close monitoring should be applied to patients with impaired liver function.
Rarely, ACE inhibitors have been associated with a syndrome that starts with cholestatic jaundice or hepatitis and progresses to fulminant hepatic necrosis and (sometimes) death. The mechanism of this syndrome is not understood. Patients receiving ACE inhibitors who develop jaundice or marked elevations of hepatic enzymes should discontinue the ACE inhibitor and receive appropriate medical follow-up.
Cases of oedema in the face, lips, tongue, glottis and/or larynx as well as the extremities have been reported in patients treated with an ACE inhibitor, including trandolapril. Angio oedema may occur particularly during the early weeks of treatment. Seldom does it develop only after prolonged treatment with an ACE inhibitor.
In such cases the trandolapril treatment should be discontinued immediately, and the patient monitored until the oedema disappears. When the oedema is localised to include only the face, it generally disappears without treatment, although antihistamines have been useful in relieving symptoms.
The combination of facial and glottis oedema may be life-threatening. Swelling of the tongue, glottis or larynx may cause respiratory obstruction. Subcutaneous adrenaline 0.1% (0.3-0.5 ml) must be given rapidly and other therapeutic measures taken as appropriate. Caution must be exercised in patients with a history of idiopathic angioedema, and trandolapril is contraindicated if angioedema was an adverse reaction to an ACE inhibitor (see section 4.3).
After such a reaction treatment with an ACE inhibitor must not be resumed. Patients with prior Quincke’s oedema not occurring in connection with ACE inhibitor treatment run a greater risk of a new Quincke’s oedema if they are treated with an ACE inhibitor (see section 4.3).
It has been shown that ACE inhibitors cause a higher rate of angioedema in black than in non black patients.
Concomitant use of ACE inhibitors with sacubitril/valsartan is contraindicated due to the increased risk of angioedema (see section 4.3). Treatment with sacubitril/valsartan must not be initiated earlier than 36 hours after the last dose of trandolapril. Treatment with trandolapril must not be initiated earlier than 36 hours after the last dose of sacubitril/valsartan (see sections 4.3 and 4.5). Concomitant use of other NEP inhibitors (e.g. racecadotril) and ACE inhibitors may also increase the risk of angioedema (see section 4.5). Hence, a careful benefit-risk assessment is needed before initiating treatment with NEP inhibitors (e.g. racecadotril) in patients on trandolapril.
Intestinal angioedema has been reported in patients treated with ACE inhibitors. These patients presented with abdominal pain (with or without nausea or vomiting); in some cases there was no prior facial angioedema and C-1 esterase levels were normal. The angioedema was diagnosed by procedures including abdominal CT scan, or ultrasound or at surgery and symptoms resolved after stopping the ACE inhibitor. Intestinal angioedema should be included in the differential diagnosis of patients on ACE inhibitors presenting with abdominal pain (see section 4.8).
Concomitant use of ACE inhibitors with racecadotril, mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) and vildagliptin may lead to an increased risk of angioedema (e.g. swelling of the airways or tongue, with or without respiratory impairment) (see section 4.5). Caution should be used when starting racecadotril, mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) and vildagliptin in a patient already taking an ACE inhibitor.
As is the case with other ACE inhibitors, trandolapril may be less effective lowering blood pressure in black than in non black patients. This may possibly be due to a higher incidence of low renin conditions in hypertensive black patients.
During treatment with an ACE inhibitor, a dry and non-productive cough may occur which disappears after discontinuation. If treatment with an ACE inhibitor is considered essential, a resumption of treatment may be considered.
ACE inhibitor-induced cough should be considered as part of the differential diagnosis of cough.
ACE inhibitors can cause hyperkalemia because they inhibit the release of aldosterone. The effect is usually not significant in patients with normal renal function. However, in patients with impaired renal function and/or in patients taking potassium supplements (including salt substitutes), potassium-sparing diuretics, trimethoprim or co-trimoxazole also known as trimethoprim/sulfamethoxazole and especially aldosterone antagonists or angiotensin-receptor blockers, hyperkalemia can occur. Potassium-sparing diuretics and angiotensin-receptor blockers should be used with caution in patients receiving ACE inhibitors, and serum potassium and renal function should be monitored (see section 4.5).
Risk factors for the development of hyperkalemia include renal insufficiency, worsening of the renal condition, age (>70 years), diabetes mellitus, intercurrent events, in particular dehydration, left ventricular dysfunction after myocardial infarction, metabolic acidosis, and concomitant use of potassium-sparing diuretics (e.g. spironolactone, eplerenone, triamterene, or amiloride), potassium supplements or potassium- containing salt substitutes; or those patients taking other drugs associated with increases in serum potassium (e.g. heparin, co-trimoxazole also known as trimethoprim/sulfamethoxazole). Hyperkalaemia can cause serious, sometimes fatal arrhythmias.
In patients undergoing major surgery or during anaesthesia with potentially hypotensive agents, ACE inhibitors including trandolapril may block angiotensin II formation secondary to compensatory renin release which may induce a possibly severe arterial hypotension, which can be corrected with plasma expanders. If it is not possible to discontinue treatment with the ACE inhibitor, volume therapy should be given with care.
ACE inhibitors should not be used in patients with aortic stenosis or obstructed outflow from the left ventricle.
In patients on ACE inhibitors, neutropenia/agranulocytosis and bone marrow depression have been seen. These reactions are more frequent in patients with patients with renal impairment, especially those with a collagen vascular disease (e.g. lupus erythematosus disseminatus and scleroderma), as well as immunosuppressive therapy with agents having a potential risk of leucopenia. Neutropenia is reversible after discontinuation of the ACE inhibitor. The best prevention is to keep carefully to the recommended dose. If treatment with an ACE inhibitor is deemed necessary in such risk patients, the risk/benefit ratio must be considered carefully. Regular monitoring of the white blood cell counts and protein in the urine must be considered in patients with collagen vascular diseases (e.g. lupus erythematosus and scleroderma), especially associated with impaired renal function and concomitant therapy, particularly with corticosteroids and antimetabolites, or treatment with allopurinol or procainamide.
Proteinuria may occur particularly in patients with existing renal function impairment or relatively high doses of ACE inhibitors. Trandolapril should only be administered after critical evaluation of the risk/benefit of treatment of patients with clinically relevant proteinuria (more than 1 g/day).
Rarely, patients receiving ACE inhibitors during desensitisation with animal venom have experienced life-threatening anaphylactoid reactions. These reactions were avoided by temporarily withholding ACE inhibitor therapy prior to each desensitisation.
Rarely, patients receiving ACE inhibitors during low density lipoprotein (LDL)-apheresis with dextran sulphate have experienced life-threatening anaphylactoid reactions. These reactions were avoided by temporarily withholding ACE-inhibitor therapy prior to each apheresis.
Anaphylactoid reactions such as facial flushing, hypotension and dyspnoea have been reported in patients dialysed with high-flux membranes (e.g. AN 69) and treated concomitantly with an ACE inhibitor. In these patients consideration should be given to using a different type of dialysis membrane or a different class of antihypertensive agent.
In diabetic patients treated with oral antidiabetic agents or insulin, glycaemic control should be closely monitored during the first month of treatment with an ACE inhibitor (see section 4.5).
ACE inhibitors should not be initiated during pregnancy. Unless continued ACE inhibitor therapy is considered essential, patients planning pregnancy should be changed to alternative anti-hypertensive treatments which have an established safety profile for use in pregnancy. When pregnancy is diagnosed, treatment with ACE inhibitors should be stopped immediately, and, if appropriate, alternative therapy should be started (see sections 4.3 and 4.6).
The safety and efficacy of trandolapril in children have not been studied.
This medicinal product IS GENERALLY NOT RECOMMENDED in combination with potassium-sparing diuretics, potassium salts and lithium (see section 4.5).
There is evidence that the concomitant use of ACE-inhibitors, angiotensin II receptor blockers or aliskiren increases the risk of hypotension, hyperkalaemia and decreased renal function (including acute renal failure). Dual blockade of RAAS through the combined use of ACE-inhibitors, angiotensin II receptor blockers or aliskiren is therefore not recommended (see sections 4.5 and 5.1).
If dual blockade therapy is considered absolutely necessary, this should only occur under specialist supervision and subject to frequent close monitoring of renal function, electrolytes and blood pressure.
ACE-inhibitors and angiotensin II receptor blockers should not be used concomitantly in patients with diabetic nephropathy.
Patients with rare hereditary problems of galactose intolerance, Lapp lactase deficiency, or glucose- galactose malabsorption should not take this medicine.
Concomitant use of ACE inhibitors with sacubitril/valsartan is contraindicated as this increases the risk of angioedema (see section 4.3 and 4.4).
Concomitant use of ACE inhibitors with racecadotril, mTOR inhibitors (e.g. sirolimus, everolimus, temsirolimus) and vildagliptin may lead to an increased risk for angioedema (see section 4.4).
The concomitant use of trandolapril with sacubitril/valsartan is contraindicated, as the concomitant inhibition of neprilysin (NEP) and ACE may increase the risk of angioedema. Sacubitril/valsartan must not be started until 36 hours after taking the last dose of trandolapril therapy. Trandolapril therapy must not be started until 36 hours after the last dose of sacubitril/valsartan (see sections 4.3 and 4.4). Concomitant use of other NEP inhibitors (e.g. racecadotril) and trandolapril may also increase the risk of angioedema (see section 4.4).
Although serum potassium usually remains within normal limits, hyperkalaemia may occur in some patients treated with trandolapril. Potassium sparing diuretics (e.g. spironolactone, triamterene, or amiloride), potassium supplements, or potassium-containing salt substitutes may lead to significant increases in serum potassium. Care should also be taken when trandolapril is co-administered with other agents that increase serum potassium, such as trimethoprim and cotrimoxazole (trimethoprim/sulfamethoxazole) as trimethoprim is known to act as a potassium-sparing diuretic like amiloride. Therefore, the combination of trandolapril with the above-mentioned drugs is not recommended. If concomitant use is indicated, they should be used with caution and with frequent monitoring of serum potassium.
Concurrent administration of potassium or potassium-sparing diuretics increases the risk of hyperkalaemia, particularly in renal failure, diabetes mellitus, and/or left ventricular dysfunction after myocardial infarction. In the randomised placebo-controlled, parallel-group Trandolapril Cardiac Evaluation (TRACE) study in patients surviving an acute myocardial infarction with residual left ventricular systolic dysfunction hyperkalaemia was observed as an adverse event in 5% (0.2% related) and 3% subjects (none related) in the trandolapril and placebo groups, respectively. Eighty (80%) subjects in this study received diuretics (see section 4.4). Should this combination be considered necessary, frequent monitoring of serum potassium is essential.
Concomitant use may result in an increased plasma lithium concentration, potentially to toxic levels (decreases renal lithium excretion). Use of trandolapril with lithium is not recommended, but if the combination proves necessary, careful monitoring of serum lithium levels should be performed.
ACE inhibitors may potentiate the hypotensive effects of certain inhalation anaesthetic agents.
Patients in diuretic treatment, especially patients who have recently begun treatment or patients with volume and/or salt depletion, may develop a severe fall in blood pressure and/or pre-renal failure after initial treatment with an ACE inhibitor. The risk of hypotensive episodes can be reduced by discontinuing the diuretics, by increasing salt intake beforehand and by starting treatment with lower initial doses of ACE inhibitor. Further dose increase should be made with caution. Trandolapril may attenuate the potassium loss caused by thiazide-type and loop diuretics.
The combination of trandolapril and other antihypertensive agents may potentiate the antihypertensive response to ACE inhibitors.
Clinical trial data has shown that dual blockade of the renin-angiotensin-aldosterone-system (RAAS) through the combined use of ACE-inhibitors, angiotensin II receptor blockers or aliskiren is associated with a higher frequency of adverse events such as hypotension, hyperkalaemia and decreased renal function (including acute renal failure) compared to the use of a single RAAS-acting agent (see sections 4.3, 4.4 and 5.1).
Postural hypotension may occur if administered concurrently.
If used concomitantly with ACE inhibitors, they may increase the risk of leucopoenia.
As with all antihypertensives, non-steroidal anti-inflammatory drugs (i.e. acetylsalicylic acid at anti-inflammatory dosage regimens, COX-2 inhibitors and non-selective NSAIDs) may reduce the antihypertensive effects of trandolapril. Concomitant use of ACE inhibitors and NSAIDs may lead to an increased risk of worsening of renal function, including possible acute renal failure, and an increase in serum potassium. These effects are, in principle, reversible and occur especially in patients with poor pre-existing renal function. The combination should be administered with caution, especially in older people. Patients should be adequately hydrated and consideration should be given to monitoring blood pressure and renal function after initiation or discontinuation of concomitant therapy, and periodically thereafter.
NSAIDs including acetylsalicylic acid, unless acetylsalicylic acid is used in lower doses as a platelet aggregation inhibitor, should be avoided with ACE inhibitors in patients with heart failure.
Sympathomimetics can reduce the hypotensive effect of ACE inhibitors. The patient should be closely monitored to ensure that the desired effect is achieved.
As with all ACE inhibitors, concomitant use of antidiabetic medicines (insulin or oral hypoglycaemic agents) may cause an increased blood glucose lowering effect with greater risk of hypoglycaemia. Therefore, blood glucose should be closely monitored in diabetics, particularly when starting or increasing the dose of an ACE inhibitor.
Concurrent administration may lead to reduced bioavailability of ACE inhibitors. Therefore, at least two hours should elapse between administration of trandolapril and antacids.
There is an increased risk of orthostatic hypotension, as with all other antihypertensives, in combination with neuroleptics or tricyclic antidepressants.
Hyperkalaemia may occur during concomitant use of ACE inhibitors with ciclosporin. Monitoring of serum potassium is recommended.
Hyperkalaemia may occur during concomitant use of ACE inhibitors with heparin. Monitoring of serum potassium is recommended.
There are rare reports of nitritoid reactions (symptoms include flushing of the face, nausea, vomiting and hypotension) in patients receiving concomitant injection treatment with gold (sodium aurothiomalate) and treatment with an ACE inhibitor.
Drinking alcohol increases the hypotensive effect of trandolapril.
Anaphylactoid reactions to high-flux polyacrylonitrile membranes used in haemodialysis have been reported in patients treated with ACE inhibitors. As with other antihypertensives of this chemical class, this combination should be avoided when prescribing ACE inhibitors to renal dialysis patients.
In studies on healthy volunteers, pharmacokinetic interactions were not observed when trandolapril was combined with digoxin, furosemide, nifedipin, glibenclamide, propranolol or cimetidin. The anticoagulant properties of warfarin were not affected after concurrent administration of trandolapril.
Clinical interactions were not observed in patients with left ventricular dysfunction after acute myocardial infarction when trandolapril was administered concurrently with thrombolytics, acetylsalicylic acid, beta blockers, calcium antagonists, nitrates, anticoagulants, diuretics or digoxin.
Interaction studies have only been performed in adults.
The use of ACE inhibitors is not recommended during the first trimester of pregnancy (see section 4.4). The use of ACE inhibitors is contra-indicated during the second and third trimester of pregnancy (see section 4.3 and 4.4)
Epidemiological evidence regarding the risk of teratogenicity following exposure to ACE inhibitors during the first trimester of pregnancy has not been conclusive; however a small increase in risk cannot be excluded. Unless continued ACE inhibitor therapy is considered essential, patients planning pregnancy should be changed to alternative anti-hypertensive treatments which have an established safety profile for use in pregnancy. When pregnancy is diagnosed, treatment with ACE inhibitors should be stopped immediately, and, if appropriate, alternative therapy should be started.
Exposure to ACE inhibitor therapy during the second and third trimesters is known to induce human foetotoxicity (decreased renal function, oligohydramnios, skull ossification retardation) and neonatal toxicity (renal failure, hypotension, hyperkalaemia) (see section 5.3). Should exposure to ACE inhibitor have occurred from the second trimester of pregnancy, ultrasound check of renal function and skull is recommended. Infants whose mothers have taken ACE inhibitors should be closely observed for hypotension (see sections 4.3 and 4.4).
Because no information is available regarding the use of trandolapril during breast-feeding, trandolapril is not recommended and alternative treatments with better established safety profiles during breast-feeding are preferable, especially while nursing a newborn or preterm infant.
Given the pharmacological properties of trandolapril, no particular effect is expected.
Due to individual differences in reaction to an ACE inhibitor, the ability to drive or operate machinery may be reduced due to the side effects seen such as dizziness and fatigue.
This may occur particularly at the start of treatment or when changing over from other medication, after increases in dose or during concurrent use of alcohol. Therefore, after the first dose or subsequent increases in dose, it is not advisable to drive or operate machinery for several hours.
The following table displays adverse reactions reported in hypertension (n=2,520) and post-myocardial infarction (n=876) clinical trials and from post-marketing experience with trandolapril.
Within each frequency grouping, adverse reactions are presented in order of decreasing seriousness, when the seriousness could be assessed.
Undesirable side effects are listed below using the following convention:
Very common (≥1/10)
Common (≥1/100 to <1/10)
Uncommon (≥1/1,000 to <1/100)
Rare (≥1/10,000 to <1/1,000)
Very rare (<1/10,000)
Not known (cannot be estimated from the available data)
Uncommon: Upper respiratory tract infection.
Rare: Urinary tract infection, bronchitis, pharyngitis.
Rare: Leucopenia, anaemia, platelet disorder, white blood cell disorder.
Not known: Agranulocytosis, pancytopenia, platelet count decreased, haemoglobin decreased, haematocrit decreased.
Rare: Hypersensitivity.
Rare: Hyperglycaemia, hyponatraemia, hypercholesterolaemia, hyperlipidaemia, hyperuricaemia, gout, anorexia, increased appetite, enzyme abnormality.
Not known: Hyperkalaemia
Uncommon: Insomnia, libido decreased.
Rare: Hallucination, depression, sleep disorder, anxiety, agitation, apathy, nervousness.
Common: Headache, dizziness
Uncommon: Somnolence
Rare: Cerebrovascular accident, syncope, myoclonus, paraesthesia, migraine, migraine without aura, dysgeusia
Not known: Transient ischaemic attack, cerebral haemorrhage, balance disorder
Rare: Blepharitis, conjunctival oedema, visual impairment, eye disorder
Uncommon: Vertigo
Rare: Tinnitus
Uncommon: Palpitations
Rare: Myocardial infarction, myocardial ischaemia, angina pectoris, cardiac failure, ventricular tachycardia, tachycardia, bradycardia
Not known: Atrioventricular block, cardiac arrest, arrhythmia, electrocardiogram abnormal
Common: Hypotension*
Uncommon: Hot flushes
Rare: Hypertension, angiopathy, orthostatic hypotension, peripheral vascular disorder, varicose vein
Not known: Cerebrovascular infarction
Common: Cough
Uncommon: Upper respiratory tract inflammation, upper respiratory tract congestion
Rare: Dyspnoea, epistaxis, pharyngeal inflammation, oropharyngeal pain, productive cough, respiratory disorder, throat irritation, rhinorrhoea.
Not known: Bronchospasm
Uncommon: Nausea, diarrhoea, constipation, gastro-intestinal pain, gastro-intestinal disorder
Rare: Haematemesis, gastritis, vomiting, abdominal pain, dyspepsia, dry mouth, flatulence.
Not known: Ileus, pancreatitis
Rare: Hepatitis, hyperbilirubinaemia
Very rare: Cholestasis
Not known: Jaundice, liver function test abnormal, transaminases increased
Uncommon: Pruritus, skin rash
Rare: Angioedema, hyperhidrosis, psoriasis, eczema, acne, dry skin, skin disorder
Very rare: Dermatitis
Not known: Urticaria, Stevens-Johnson syndrome, toxic epidermal necrolysis, alopecia.
Uncommon: Back pain, muscle spasms, pain in extremity
Rare: Myalgia, arthralgia, bone pain, osteoarthritis
Rare: Renal failure, azotaemia, polyuria, pollakiuria
Not known: Blood creatinine increased, blood urea increased, proteinuria
Uncommon: Erectile dysfunction
Rare: Congenital arterial malformation, ichthyosis
Common: Asthenia
Uncommon: Malaise, chest pain, oedema peripheral, feeling abnormal
Rare: Oedema, fatigue
Not known: Pyrexia
Very rare: Raised potassium blood levels, gamma-glutamyl transferase, raised lipase, raised immunoglobulin.
Not known: Increased serum urea, increased serum creatinine, reduced platelet count, increased liver function tests (including ASAT and ALAT), blood alkaline phosphatase increased, blood lactate dehydrogenase increased, laboratory test abnormal.
Rare: Injury
* Hypotension has a common frequency in patients with left ventricular dysfunction following myocardial infarction from the TRACE clinical study (n=876). However, it has an uncommon frequency in those patients from hypertension clinical trials (n=2,520).
Undesirable effects reported for ACE inhibitors as a class (frequency not given):
Blood and lymphatic system disorders: Haemolytic anaemia, eosinophilia and/or increased ANA (anti-nuclear antibody)
Nervous system disorders: Confusional state
Eye disorders: Vision blurred
Respiratory, thoracic and mediastinal disorders: Sinusitis, rhinitis, glossitis
Gastrointestinal disorders: Intestinal angioedema.
Skin and subcutaneous tissue disorders: Erythema multiforme, psoriasis-like efflorescences
Congenital, familial and genetic disorders: Haemolytic anaemia with a congenital deficiency concerning G-6 PDH (glucose-6-phosphate dehydrogenase).
Reporting suspected adverse reactions after authorisation 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 via www.mhra.gov.uk/yellowcard or search for MHRA Yellow Card in the Google Play or Apple App Store.
Not applicable.
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