Source: Marketing Authorisation Holder Revision Year: 2022 Publisher: Viatris Pty Ltd, Level 1, 30 The Bond, 30-34 Hickson Road, Millers Point NSW 2000, www.viatris.com.au, Phone: 1800 274 276
Fluvoxamine is contraindicated in combination with tizanidine.
Fluvoxamine should not be used in combination with monoamine oxidase inhibitors (MAOIs) or reversible MAOIs (RIMAs), moclobemide or linezolid, or within 14 days of discontinuing treatment with a MAOI. Similarly, at least one week should be allowed after stopping fluvoxamine before starting a MAOI. Cases of serious reactions, such as potentially life-threatening serotonin syndrome (characterised by neuromuscular excitation, altered mental status and autonomic dysfunction) have been reported in patients receiving an SSRI in combination with MAOIs and RIMA, and in patients who have recently discontinued an SSRI and have started on a MAOI (see Section 4.4 SPECIAL WARNINGS AND PRECAUTIONS FOR USE).
Fluvoxamine immediate-release tablets should not be used in combination with pimozide and ramelteon.
Fluvoxamine is contraindicated in combination with cisapride.
LUVOX tablets are contraindicated in patients with hypersensitivity to any component of the product (see Section 2 QUALITATIVE AND QUANTITATIVE COMPOSITION and Section 6.1 LIST OF EXCIPIENTS).
Fluvoxamine has been shown to increase postnatal mortality in rats at doses greater than 1 mg/kg/day, and should not be used by nursing mothers.
A major depressive episode may be the initial presentation of bipolar disorder. It is generally believed that treating such an episode with an antidepressant alone may increase the likelihood of precipitation of a mixed/manic episode in patients at risk of bipolar disorder. Prior to initiating treatment with an antidepressant, patients should be adequately screened to determine if they are a risk for bipolar disorder; such screening should include a detailed psychiatric history, including a family history of suicide, bipolar disorder and depression.
The risk of suicide attempt is inherent in depression and may persist until significant remission occurs. This risk must be considered in all depressed patients.
Patients with depression may experience worsening of their depressive symptoms and/or the emergence of suicidal ideation and behaviours (suicidality) whether or not they are taking antidepressant medications, and this risk may persist until significant remission occurs. As improvement may not occur during the first few weeks or more of treatment, patients should be closely monitored for clinical worsening and suicidality, especially at the beginning of a course of treatment, or at the time of dose changes, either increases or decreases. Consideration should be given to changing the therapeutic regimen, including possibly discontinuing the medication, in patients whose depression is persistently worse or whose emergent suicidality is severe, abrupt in onset, or was not part of the patient’s presenting symptoms.
Patients (and caregivers of patients) should be alerted about the need to monitor for any worsening of their condition and/or the emergence of suicidal ideation/ behaviour or thoughts of harming themselves and to seek medical advice immediately if these symptoms present. Patients with co-morbid depression associated with other psychiatric disorders being treated with antidepressants should be similarly observed for clinical worsening and suicidality.
Obsessive compulsive disorders may also be associated with an increased risk of suicide-related events. The same precautions should therefore be observed for these patients.
Patients with a history of suicide-related events, or those exhibiting a significant degree of suicidal ideation prior to commencement of treatment, are at a greater risk of suicidal thoughts or suicide attempts, and should receive careful monitoring during treatment.
Pooled analyses of 24 short-term (4 to 16 weeks), placebo-controlled trials of nine antidepressant medicines (SSRIs and others) in 4400 children and adolescents with major depressive disorder (16 trials), obsessive compulsive disorder (4 trials), or other psychiatric disorders (4 trials) have revealed a greater risk of adverse events representing suicidal behaviour or thinking (suicidality) during the first few months of treatment in those receiving antidepressants. The average risk of such events in patients treated with an antidepressant was 4%, compared with 2% of patients given placebo. There was considerable variation in risk among the antidepressants, but there was a tendency towards an increase for almost all antidepressants studied. The risk of suicidality was most consistently observed in the major depressive disorder trials, but there were signals of risk arising from trials in other psychiatric indications (obsessive compulsive disorder and social anxiety disorder) as well. No suicides occurred in these trials. It is unknown whether the suicidality risk in children and adolescent patients extends to use beyond several months. The nine antidepressant medicines in the pooled analyses included five SSRIs (citalopram, fluoxetine, fluvoxamine, paroxetine, sertraline) and four non-SSRIs (bupropion, mirtazapine, nefazodone, venlafaxine).
Pooled analysis of short-term studies of antidepressant medications have also shown an increased risk of suicidality in young adults aged 18 to 24 during initial treatment (generally the first one to two months). Shortterm studies did not show an increase in the risk of suicidality with antidepressants compared to placebo in adults beyond the age of 24 years; there was a reduction with antidepressants compared to placebo in adults aged 65 years and older.
Symptoms of anxiety, agitation, panic attacks, insomnia, irritability, hostility (aggressiveness), impulsivity, akathisia (psychomotor restlessness), hypomania, and mania, have been reported in adults, adolescents and children being treated with antidepressants for major depressive disorder as well as for other indications, both psychiatric and non-psychiatric. Although a causal link between the emergence of such symptoms and either worsening of depression and/or emergence of suicidal impulses has not been established, there is concern that such symptoms may be precursors of emerging suicidality.
Families and caregivers of children and adolescents being treated with antidepressants for major depressive disorder or for any other condition (psychiatric or non-psychiatric) should be informed about the need to monitor these patients for the emergence of agitation, irritability, unusual changes in behaviour, and other symptoms described above, as well as the emergence of suicidality, and to report such symptoms immediately to health care providers. It is particularly important that monitoring be undertaken during the initial few months of antidepressant treatment or at times of dose increase or decrease.
Prescriptions of LUVOX should be written for the smallest quantity of tablets consistent with good patient management, in order to reduce the risk of overdose.
The use of fluvoxamine has been associated with the development of akathisia. This is most likely to occur within the first few weeks of treatment. In patients who develop these symptoms, increasing the dose may be detrimental.
The presentation of akathisia may be variable and comprises subjective complaints of restlessness and an overwhelming urge to move and either distress or motor phenomena such as pacing, swinging of the legs while seated, rocking from foot to foot, or both. Particular attention should be paid to the monitoring for such symptoms and signs as, left untreated, akathisia is associated with poor compliance and an increased risk of relapse.
Although in animal studies, fluvoxamine has no pro-convulsive properties, caution is recommended when the drug is administered to patients with a history of convulsive disorders. Fluvoxamine should be avoided in patients with unstable epilepsy and patients with controlled epilepsy should be carefully monitored. Treatment with fluvoxamine should be discontinued if seizures occur or if seizure frequency increases.
As with other SSRIs, hyponatraemia has been rarely reported, and appears to be reversible when fluvoxamine is discontinued. Some cases were possibly due to the syndrome of inappropriate antidiuretic hormone secretion. The majority of reports were associated with older patients. Glycaemic control may be disturbed (i.e. hyperglycaemia, hypoglycaemia, decreased glucose tolerance), especially in the early stages of treatment. When fluvoxamine is given to patients with a known history of diabetes mellitus, the dosage of anti-diabetic drugs may need to be adjusted.
Mydriasis has been reported in association with SSRIs such as fluvoxamine. Therefore, caution is recommended when prescribing fluvoxamine for patients with raised intraocular pressure or those at risk of acute narrow-angle glaucoma.
There have been reports of cutaneous bleeding abnormalities such as ecchymoses and purpura as well as other haemorrhagic manifestations such as gastrointestinal bleeding or gynaecological haemorrhage with SSRIs. Caution is advised in patients taking SSRIs, particularly in elderly patients and in patients who concomitantly use drugs known to affect platelet function (e.g. atypical antipsychotics and phenothiazines, most tricyclic antidepressants, aspirin and NSAIDs) or drugs that increase risk of bleeding as well as in patients with a history of bleeding disorders and in those with predisposing conditions (e.g. thrombocytopenia, or coagulation disorders). If any significant bleeding or bruising is observed, it is recommended that a platelet count should be performed.
When combined with fluvoxamine, plasma concentrations of terfenadine, astemizole or cisapride may be increased, resulting in an increased risk for QT-prolongation/Torsades de pointes. Therefore, fluvoxamine should not be co-administered with these agents. Fluvoxamine may cause an insignificant decrease in heartbeat (2-6 beats per minute).
Serious skin reactions, some of them fatal, including Stevens-Johnson syndrome and toxic epidermal necrolysis, have been reported in association with fluvoxamine (see Section 4.8 ADVERSE EFFECTS (UNDESIRABLE EFFECTS)). Patients appear to be at highest risk of these reactions early in the course of therapy. If skin reactions occur, fluvoxamine should be discontinued immediately, and the patient should be closely monitored.
There is limited clinical experience of concomitant administration of fluvoxamine and ECT; therefore, caution is advisable.
Development of serotonin syndrome or neuroleptic malignant syndrome-like events may occur in association with treatment with SSRIs, particularly when given in combination with MAOIs or other serotonergic and/or neuroleptic agents or in combination with opiate/opioid drugs (e.g. buprenorphine) or in combination with the fixed-dose combination preparation buprenorphine/naloxone. Symptoms and signs of serotonin syndrome include rapid onset of neuromuscular excitation (hyperreflexia, incoordination, myoclonus, tremor), altered mental status (confusion, agitation, hypomania) and autonomic dysfunction (diaphoresis, diarrhoea, fever, shivering and rapidly fluctuating vital signs). Treatment with fluvoxamine should be discontinued if such events occur and supportive symptomatic treatment initiated.
The onset of symptoms may occur one to three days after abrupt discontinuation of SSRI therapy and (rarely) after dosage lowering. It is important but may be difficult to distinguish the discontinuation symptoms from a recurrence of the underlying disease. Both may present with disturbances of the equilibrium and of the sensory system. However, they may differ in view of the severity, onset and duration of the symptoms.
Discontinuation symptoms rarely occur after treatment of less than 5 weeks' duration and usually last from one day to three weeks.
The most commonly reported symptoms in association with withdrawal of the medicine include: dizziness, sensory disturbances (including paraesthesia, visual disturbances and electric shock sensations), sleep disturbances (including insomnia and intense dreams), agitation, irritability, confusion, emotional stability, headache, nausea and/or vomiting, diarrhoea, sweating, palpitations, tremor and anxiety (see Section 4.8 ADVERSE EFFECTS (UNDESIRABLE EFFECTS)). Generally, these effects are mild to moderate and are self-limiting; however, in some patients they may be severe and/or prolonged. They usually occur within the first few days of discontinuing treatment.
It is advised that in accordance with clinical experience and individual need of a patient the dosage should be gradually tapered over a couple of weeks when discontinuing treatment (see Section 4.2 DOSE AND METHOD OF ADMINISTRATION).
Fluvoxamine should be used with caution in patients with a history of mania/hypomania. Fluvoxamine should be discontinued in any patient entering a manic phase.
Patients suffering from hepatic insufficiency should start on a low dose and be carefully monitored when treated with fluvoxamine. Upward dose titration should be carried out more slowly in this patient population. Clearance of fluvoxamine is slower in patients with hepatic impairment (e.g. cirrhosis).
Treatment with fluvoxamine has rarely been associated with an increase in hepatic enzymes, generally accompanied by clinical symptoms. In such cases, treatment should be discontinued.
Patients suffering from renal insufficiency should start on a low dose and be carefully monitored when treated with fluvoxamine. Upward dose titration should be carried out more slowly in this patient population
Data in elderly subjects gives no indication of clinically significant differences in pharmacokinetics compared with younger subjects. Nevertheless, upward dose titration should be carried out more slowly in this patient population, and dosing should always be handled with caution.
Fluvoxamine should not be used in children and adolescents (age <18 years) for the treatment of major depressive disorder as the efficacy and safety of the medicine in these patients for this condition has not been satisfactorily investigated.
Decreased appetite and weight loss have been observed in association with the use of fluvoxamine as well as with other SSRIs. Although no detrimental effect on growth, development and maturation was apparent in the long-term, open-label clinical studies in children, regular monitoring of weight and growth is recommended if treatment of a child with an SSRI is to be continued long term.
Rarely, treatment with fluvoxamine has been associated with an increase in hepatic enzymes, mostly accompanied by clinical symptoms. In these cases, treatment should be discontinued.
Effects on other laboratory tests have not been established.
The concurrent use of fluvoxamine with tizanidine, or cisapride is contraindicated (see Section 4.3 CONTRAINDICATIONS).
Fluvoxamine immediate-release tablets should not be used in combination with ramelteon (see Section 4.3 CONTRAINDICATIONS).
The serotonergic effects of fluvoxamine may be enhanced when used in combination with other serotonergic agents and/or neuroleptic drugs including opioid preparations (e.g. tramadol, buprenorphine and buprenorphine/naloxone), triptans, SSRIs and St John’s Wort preparations. In rare cases, this could lead to the development of a serotonin syndrome or neuroleptic malignant syndrome (NMS)-like events. As these syndromes may result in potentially life-threatening conditions, treatment with fluvoxamine should be discontinued if such events (characterised by clusters of symptoms such as hyperthermia, rigidity, myoclonus, autonomic instability with possible rapid fluctuations of vital signs, mental status changes including confusion, hypomania, extreme agitation progressing to delirium and coma) occur and supportive symptomatic treatment should be initiated.
Fluvoxamine should not be used in combination with monoamine oxidase inhibitors (MAOIs), including linezolid, due to risk of serotonin syndrome (see Section 4.3 CONTRAINDICATIONS). It should be used with caution in combination with other SSRIs, tricyclic antidepressants, tryptophan, triptans, phentermine, tramadol or opioid preparations.
Although fluvoxamine has been used in combination with lithium in the treatment of severely ill, drugresistant patients, possible potentiation of serotonergic effect should be kept in mind.
As with other psychotropic drugs, patients should be advised to avoid using alcohol while taking fluvoxamine.
When fluvoxamine was co-administered with warfarin for 2 weeks, plasma prothrombin times were prolonged. This can be ascribed to the intrinsic ability of SSRIs to lower the serotonin concentration in blood platelets (which can lead to prolonged bleeding in sensitive patients), and to fluvoxamine increasing the warfarin plasma concentrations (see below). As the risk for haemorrhage may increase, patients receiving anticoagulants should have their prothrombin time monitored and their anticoagulant dose adjusted accordingly when administered fluvoxamine.
Fluvoxamine is metabolised in the liver, mostly via the cytochrome P450 system. While the specific enzymes involved are not definitively known, it would appear, based on available in vitro data, that CYP1A2 is the main isoenzyme involved. To a much lesser extent, CYP3A4 and CYP2C19 may also be involved in the metabolism of fluvoxamine.
In addition, fluvoxamine can inhibit the metabolism of drugs metabolised by certain P450 isoenzymes. A strong inhibition of CYP1A2 and CYP2C19 is demonstrated in in vitro and in vivo studies. CYP2C9, CYP2D6 and CYP3A4 are inhibited to a lesser extent.
Fluvoxamine increases or decreases (e.g. in case of prodrugs like clopidogrel) the plasma concentrations of active substance/metabolites of drugs which are largely metabolised via these isoenzymes.
Fluvoxamine has only a weak inhibitory effect on CYP2D6, and is therefore not likely to increase plasma concentrations of drugs metabolised by CYP2D6 to a clinically relevant extent.
Concomitant therapy of fluvoxamine and these drugs should be initiated at or adjusted to the low end of their dosage range. Plasma concentrations, effects or adverse effects of co-administered drugs should be monitored and their dosage should be reduced if necessary. This is particularly relevant for drugs with a narrow therapeutic index.
An increase in previously stable plasma levels of those tricyclic antidepressants (such as clomipramine, amitriptyline and imipramine) and neuroleptics (or antipsychotics such as clozapine, olanzapine, quetiapine) which are largely metabolized through CYP1A2 has been reported when used together with fluvoxamine. The combination of fluvoxamine with these drugs is not recommended.
Patients co-administered fluvoxamine and CYP1A2 metabolised drugs with a narrow therapeutic index (such as tacrine, theophylline, methadone, mexiletine, phenytoin, carbamazepine and ciclosporin) should be carefully monitored when these agents are metabolized exclusively or by a combination of CYPs inhibited by fluvoxamine. If necessary, dose adjustment of these drugs is recommended.
Due to the narrow therapeutic index of pimozide and its known ability to prolong QT interval, concomitant use of pimozide and fluvoxamine is contraindicated (see Section 4.3 CONTRAINDICATIONS).
Isolated cases of cardiac toxicity have been reported when fluvoxamine was combined with thioridazine. Caffeine plasma levels are likely to be increased during co-administration with fluvoxamine. Thus, patients who consume high quantities of caffeine-containing beverages should lower their intake when fluvoxamine is administered and adverse caffeine effects (like tremor, palpitations, nausea, restlessness, insomnia) are observed.
Side effects may be increased when fluvoxamine is used in combination with terfenadine, astemizole, cisapride and sildenafil (see Section 4.4 SPECIAL WARNINGS AND PRECAUTIONS FOR USE).
When combined with fluvoxamine, plasma concentrations of cisapride may be increased, resulting in an increased risk of QT-prolongation/Torsades de pointes. Therefore, fluvoxamine should not be coadministered with cisapride.
The plasma concentrations of benzodiazepines metabolised by oxidation (such as triazolam, midazolam, alprazolam and diazepam) are likely to increase when co-administered with fluvoxamine. The dosages of these benzodiazepines should be reduced during co-administration with fluvoxamine. For benzodiazepines metabolised by glucuronidation (lorazepam, lormetazepam, oxazepam, temazepam) or nitro-reduction (clonazepam, nitrazepam) such an effect is not likely to occur.
Increased serum concentrations of haloperidol have also been reported after concomitant use of haloperidol and fluvoxamine.
Patients co-administered fluvoxamine and CYP3A4 metabolised drugs with a narrow therapeutic index (e.g. ciclosporin, methadone or carbamazepine) should be carefully monitored and, if necessary, dose adjustments of these drugs is recommended.
Patients co-administered fluvoxamine and CYP2C metabolised drugs with a narrow therapeutic index (such as phenytoin) should be carefully monitored and, if necessary, dose adjustments of these drugs is recommended.
As plasma concentrations of ropinirole may be increased in combination with fluvoxamine thus increasing the risk of overdose, surveillance and reduction in the dosing of ropinirole during fluvoxamine treatment and after its withdrawal may be required.
As plasma concentrations of propranolol are increased in combination with fluvoxamine, the propranolol dose may need to be lowered.
When given with fluvoxamine, warfarin plasma concentrations were significantly increased and prothrombin time prolonged.
No interactions were seen with digoxin or atenolol, which are renally excreted.
After a single oral dose, fluvoxamine plasma concentrations were lower in smokers than in non-smokers.
No evidence of impairment of fertility in male or female rats was observed with fluvoxamine at oral doses up to 80 mg/kg/day.
Reproduction studies in animals revealed impaired fertility (note: at doses exceeding 2 times the maximum recommended human dosage), increased embryofoetal death, decreased foetal body weight and increased incidences of foetal eye abnormalities (folded retina) in fluvoxamine doses which markedly exceed maximum recommended human dose.
The potential risk for humans is unknown.
Fluvoxamine should not be used in patients attempting to conceive unless the clinical condition of the patient requires treatment with fluvoxamine.
Epidemiological data have suggested that the use of selective serotonin reuptake inhibitors (SSRIs) in pregnancy, particularly in late pregnancy, may increase the risk of persistent pulmonary hypertension in the newborn (PPHN). The observed risk was approximately 5 cases per 100 pregnancies. In the general population 1 to 2 cases of PPHN occur per 1000 pregnancies.
There was no evidence of teratogenic effects following administration of fluvoxamine at oral doses up to 80 mg/kg/day to rats and rabbits during the period of organogenesis, with rat exposure (based on plasma AUC similar to human exposure at the maximum recommended human dose. Oral administration of fluvoxamine to rats at doses of 5-160 mg/kg/day during late gestation and lactation was associated with increased postnatal pup mortality.
Fluvoxamine should not be used during pregnancy unless the clinical condition of the woman requires such treatment. Cases of withdrawal symptoms in the newborn child have been described after the use of fluvoxamine at the end of pregnancy. Neonates exposed to LUVOX, other SNRIs (Serotonin and Norepinephrine Reuptake Inhibitors), or SSRIs (Selective Serotonin Reuptake Inhibitors), late in the third trimester have developed complications requiring prolonged hospitalization, respiratory support, and tube feeding. Such complications can arise immediately upon delivery. Reported clinical findings have included respiratory distress, cyanosis, apnea, seizures, temperature instability, feeding difficulty, vomiting, hypoglycaemia, hypotonia, hypertonia, hyperreflexia, tremor, jitteriness, lethargy, somnolence, difficulty in sleeping, irritability and constant crying. These features are consistent with either a direct effect of SSRIs and SNRIs or, possibly, a drug discontinuation syndrome.
Oral administration of fluvoxamine to rats at doses greater than 1 mg/kg/day during late gestation and lactation was associated with increased postnatal pup mortality. Since fluvoxamine is excreted in human milk, the drug should not be used by lactating women (see Section 4.3 CONTRAINDICATIONS).
Fluvoxamine at doses up to 150 mg per day exhibited no effect on psychomotor skills associated with driving and operating machinery in healthy volunteers. However, somnolence has been reported during treatment with fluvoxamine. Therefore, caution is recommended until the individual response to the drug has been determined.
Nausea, sometimes accompanied by vomiting, is the most frequently observed symptom associated with fluvoxamine treatment. This side effect usually diminishes within the first two weeks of treatment. Other adverse events, observed in clinical studies at frequencies listed below (database size approx. - 35,000 patients; dose range 50-300 mg/day), are often associated with the illness and are not necessarily related to treatment.
Events are listed within body systems and categorised by frequency according to the following definitions: Frequency estimate: Very common (>10%) Common (>1 and <10%), Uncommon (≥0.1% and <1%), Rare (≥0.01% and <0.1%), Very rare (<0.01%), Not known (cannot be estimated from the available data).
Table 1. Undesirable effects:
| MedDra system organ class | Common | Uncommon | Rare | Very rare | Frequency not known |
|---|---|---|---|---|---|
| Endocrine disorders | Hyperprolactina emia, inappropriate antidiuretic hormone secretion\ | ||||
| Metabolism and nutrition disorders | Anorexia | Hyponatraemia, weight increased, weight decreased | |||
| Psychiatric disorders | Hallucination, confusional stage, aggression | Mania | Suicidal ideation, suicidal behaviour | ||
| Nervous system disorders | Agitation, nervousness, anxiety, insomnia, somnolence, tremor, headache, dizziness | Extrapyramidal disorder, ataxia | Convulsion | Serotonin syndrome, neuroleptic malignant syndrome-like events, akathisia/psych omotor restlessness, paraesthesia, dysgeusia | |
| Eye disorders | Glaucoma, mydriasis | ||||
| Cardiac disorders | Palpitations/tachycardia | ||||
| Vascular disorders | (Orthostatic) hypotension | Haemorrhage (e.g. gastrointestinal haemorrhage, gynaecological haemorrhage, ecchymosis, purpura) | |||
| Gastrointestinal disorders | Abdominal pain, constipation, diarrhoea, dry mouth, dyspepsia, nausea, vomiting | ||||
| Hepatobiliary disorders | Hepatic function abnormal | ||||
| Skin and subcutaneous disorders | Hyperhidrosis | Cutaneous hypersensitivity reactions (including angioneurotic oedema, rash, pruritis) | Photosensitivity reaction | Steven-Johnson syndrome/toxic epidermal necrolysis | |
| Musculoskeleta l, connective tissue and bone disorders | Arthralgia, myalgia | Bone fractures* | |||
| Renal and Urinary disorders | Micturition disorder (including urinary retention, urinary incontinence, pollakiuria, nocturia and enuresis) | ||||
| Reproductive system and breast disorders | Abnormal (delayed) ejaculation | Galactorrhoea | Anorgasmia, menstrual disorders (such as amenorrhoea, hypomenorrhoea, metrorrhagia, menorrhagia) | ||
| General disorders and administration site reactions | Asthenia, malaise | Drug withdrawal syndrome including drug withdrawal syndrome neonatal |
* Epidemiological studies, mainly conducted in patients 50 years of age and older, show an increased risk of bone fractures in patients receiving SSRIs and TCAs. The mechanism leading to this risk is unknown.
Withdrawal symptoms seen on discontinuation of fluvoxamine treatment
Discontinuation of fluvoxamine treatment (particularly when abrupt) commonly leads to withdrawal symptoms. It is therefore advised that when fluvoxamine treatment is no longer required, gradual discontinuation by dose tapering should be carried out (see Section 4.2 DOSE AND METHOD OF ADMINISTRATION and Section 4.4 SPECIAL WARNINGS AND PRECAUTIONS FOR USE).
Haemorrhage ecchymoses, purpura and gastrointestinal bleeding have been reported (see Section 4.4 SPECIAL WARNINGS AND PRECAUTIONS FOR USE).
Changes in weight (weight gain or weight loss), and hyperprolactinaemia have also been reported.
Very rarely, paresthesia, taste perversion, visual disturbance and hepatitis have been reported.
Urogenital: Very rare – anorgasmia and impotence
Skin: Uncommon – cutaneous hypersensitivity reaction (including angioedema)
Reproductive system and breast disorders: Anorgasmia, menstrual disorders (such as amenorrhea, hypomenorrhea, metrorrhagia, menorrhagia)
Epidemiological studies, mainly conducted in patients 50 years of age and older, show an increased risk of bone fractures in patients receiving SSRIs and TCAs. The mechanism leading to this risk is unknown.
In paediatric patients (N=57) treated with fluvoxamine the overall profile of adverse events was generally similar to that seen in adult studies. However, the following events not appearing above have been reported in two or more of the paediatric patients and were more frequent with fluvoxamine than placebo: abnormal thinking, cough increase, dysmenorrhoea, emotional lability, epistaxis, hyperkinesia, infection and sinusitis.
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/reporting-problems.
Incompatibilities were either not assessed or not identified as part of the registration of this medicine.
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