This page was last updated: 2 March 2021 at 2:45 PM
This site contains general information for health professionals in NZ regarding medicines and COVID-19. The information is compiled by a multidisciplinary team including pharmacists, pharmacologists and infectious diseases experts.
Written information for patients to address questions and concerns about medicines and COVID-19 can be found at MyMedicines.
If you feel there are additional areas we need to cover, or for questions relating to specific patients, please contact us. If you cannot make contact by phone then please use email.
The global effects of COVID-19 on manufacturing plants and transportation are likely to result in disruptions to the medicine supply chain. PHARMAC are working closely with the Ministry of Health (MoH) and suppliers to help maintain medicine supply chains. See PHARMAC: Information for coronavirus/COVID-19
From 1 August 2020 pharmacists will be able to dispense a 3 month supply of most medicines.
COVID-19 continues to disrupt supply chains and manufacturing overseas. Therefore, dispensing restrictions may need to be reinstated for some medicines if supply issues arise.
Patients should be advised to keep at least a 1-2 week supply of their medicines and discouraged from stockpiling as this will contribute to supply issues.
Medicines with a one month dispensing restriction before lockdown will continue to be dispensed monthly e.g. paracetamol. A further 17 medicines are restricted due to supply issues e.g. amlodipine and ibuprofen 800 mg modified release tablets. See, PHARMAC: Dispensing frequency.
A pharmacist may use their discretion for certain people that require stat dispensing, even when there are dispensing restrictions e.g. people who have mobility issues, live rurally, are immunocompromised or are elderly.
For a list of medicines associated with supply issues, such as paracetamol, see: PHARMAC: Medicine and device supply issues
PHARMAC changed access criteria to some medicines as part of the COVID-19 response. However, pre-COVID-19 special authority criteria have been reinstated, see: PHARMAC: Medicines with amended access criteria.
For access restrictions to hydroxychloroquine, see PHARMAC: COVID-19: Hydroxychloroquine
|Remote prescribing in the community is possible by NZePS and non-NZePS methods if Ministry of Health (MoH) criteria are met (see below).|
The New Zealand ePrescription Service (NZePS) is a secure prescribing system for primary care. For general information, see MoH: NZePS.
To facilitate virtual care during the COVID-19 pandemic, a temporary exemption to the usual rules around physical signatures on prescriptions via NZePS and non-NZePS systems is in place. The Notice and the temporary waiver for non-NZePS signature exempt prescriptions has been extended and will now expire on 22 March 2021.
Prescriptions with a physical signature can be sent to pharmacies via fax and email. For details on the regulations, see MOH: Electronic Transmission of Prescriptions and to find a pharmacy email address, see Healthpoint: Pharmacy.
Medicines recommended for COVID-19
|Enoxaparin should be routinely used for thromboprophylaxis in hospitalised patients with COVID-19.|
COVID-19 induces a hypercoagulable state, particularly in severe cases. Patients have higher rates of venous thromboembolism (VTE) than many other medical conditions, although the exact incidence is not clearly defined. Predictably, incidence is highest in critically ill patients.
There are observational data in favour of low molecular weight heparin (LMWH) for VTE prophylaxis in COVID-19. There is a strong biological rationale, and stronger evidence for benefit of routine LMWH in other high-risk conditions.
Although the risks and benefits are not precisely defined, the overall data to date suggests benefit is more likely than harm. Therefore, we recommend the use of enoxaparin for thromboprophylaxis in hospitalised patients with COVID-19. The usual cautions and contraindications apply, for example renal impairment and patients with higher bleeding risk. Hospital HealthPathways gives advice on these issues, and the Medicines Information Service can be contacted for complex cases, particularly for advice on dosing.
Paracetamol is recommended first-line for symptomatic relief in COVID-19.
Paracetamol treats symptoms but does not improve clinical outcomes in COVID-19.
Paracetamol is an effective treatment for pain and fever in COVID-19. It is relatively safe and therefore recommended first-line for symptomatic relief in COVID-19. NSAIDs are appropriate for refractory symptoms (see relevant section below).
There are reports on social media that paracetamol can “cure” COVID-19. There is no scientific evidence to support this claim, or a plausible theory. Patients should be advised to use paracetamol in a supportive role, but warned that it does not protect them from serious harm from COVID-19 and is therefore not a substitute for established methods of infection control.
For information on dispensing paracetamol see PHARMAC: Paracetamol supply issue.
Evidence supports the use of corticosteroids in critically ill patients with severe COVID-19 who require oxygen or ventilation.
Evidence does not support starting corticosteroids in patients with milder COVID-19.
Patients should continue prescribed corticosteroids for chronic conditions e.g. musculoskeletal conditions, asthma and/or COPD.
A prospective meta-analysis of 7 randomised trials (n= 1703, including a subgroup of patients from the RECOVERY trial) found that 28-day all-cause mortality was lower among critically ill patients who received corticosteroids compared with those who received usual care or placebo (summary odds ratio, 0.66 [95% CI, 0.53-0.82]). Mortality benefits were similar for dexamethasone (oral or IV) and hydrocortisone (IV). Low and high dose regimens were included. See, Meta-analysis.
Preliminary findings from the dexamethasone arm of the RECOVERY trial (n=6425) found that dexamethasone (6 mg oral or IV once daily for 10 days compared to usual care) did not reduce mortality in patients not receiving respiratory support at randomisation. See, RECOVERY trial.
Patients who are using long-term oral or inhaled corticosteroids may have an increased risk of contracting coronavirus or developing more severe COVID-19 symptoms. However, patients should not stop long-term corticosteroids abruptly solely because of the current pandemic, or if they are exposed to someone with COVID-19 or develop COVID-19. Abrupt cessation is unlikely to be of benefit and more likely to cause harm e.g. adrenal crisis, uncontrolled asthma, or a flare of their condition. Wherever possible use the lowest necessary dose for the shortest period of time.
Remdesivir may reduce time to recovery in hospitalised patients with severe COVID-19 who require oxygen therapy.
An RCT (n=1062) found that patients who received remdesivir had a median recovery time of 10 days compared to 15 days for those who received placebo (rate ratio for recovery, 1.29; 95% CI, 1.12 to 1.49; P<0.001).
Another RCT (n= 397) showed the efficacy of 5-day and 10-day courses of remdesivir are similar for patients with severe COVID-19 not requiring mechanical ventilation.
Interim results from the remdesivir arm of the WHO SOLIDARITY trial (n=5475) found no difference in 28 day mortality, ventilation rate or duration of hospital stay with remdesivir compared to usual care.
PHARMAC has secured a small amount of remdesivir for use in New Zealand. It has not been approved by Medsafe and is being provided under Sections 25 & 29 of the Medicines Act.
PHARMAC has developed an access form for remdesivir.
Gilead Sciences (New Zealand) has provided a factsheet for remdesivir.
Medicines not recommended for COVID-19
|The treatment of COVID-19 is largely supportive.|
Recommended treatments are largely supportive. Non-pharmacological prevention measures (handwashing, physical distancing, etc.) are the only approved measures to prevent COVID-19.
The medicines in this section are based on a theoretical mechanism, in vitro data only, or weak observational data. None have sufficient rationale to justify use outside of a clinical trial.
Chloroquine and Hydroxychloroquine
|Chloroquine and hydroxychloroquine currently have no role in the treatment of COVID-19.|
There are now many published clinical trials investigating the use of hydroxychloroquine (HCQ) or chloroquine (CQ) for COVID-19.
The HCQ arm of the RECOVERY trial (n= 4716) found that there was no difference in 28 day mortality between the HCQ and usual care groups in hospitalised patients with COVID-19. Death at 28 days occurred in 27% of patients (421/1561) in the HCQ group and in 25% of patients (790/3155) in the usual care group (rate ratio, 1.09; 95% confidence interval, 0.97 to 1.23; P=0.15). Patients in the HCQ group had a longer duration of hospitalisation than those in the usual care group (median, 16 days versus 13 days). There was a small absolute excess of cardiac mortality of 0.4% but no difference in the incidence of new major cardiac arrhythmia among the patients who received HCQ. There was one report of torsades de pointes that was related to HCQ. See, RECOVERY trial
Two open-label RCTs, from China compared HCQ with standard care and involved 30 and 150 patients respectively. Both showed no difference in viral clearance, clinical improvement, or mortality. A trial of high dose vs. low dose CQ was stopped early due to toxicity in the high dose arm. There are also several observational trials published, with a combined total of over 3,000 patients, which show no benefit or harm for HCQ or CQ in multivariate analysis.
Overall, current evidence does not support HCQ or CQ being effective treatments for COVID-19. Inappropriate use outside of clinical trials risks unnecessary adverse effects and creating a shortage of these medicines for established indications e.g. rheumatoid arthritis. Accordingly, PHARMAC has restricted funding of HCQ to approved indications (rheumatoid arthritis, systemic or discoid lupus erythematosus, malaria).
|Azithromycin currently has no role in the management of COVID-19.|
Results from the azithromycin arm of the RECOVERY trial (n= 7763) did not find a clinical benefit or survival benefit in patients admitted to hospital with COVID-19. 22% of patients died within 28 days in both the azithromycin group (561/2582) and the usual care group (1162/5181) (p=0.50).
Azithromycin and hydroxychloroquine are QTc prolonging drugs and their combined use increases this risk. Widespread use of azithromycin increases the potential for bacterial resistance. Azithromycin use in patients admitted to hospital with COVID-19 should be restricted to patients in whom there is a clear antimicrobial indication.
Most antivirals currently have no role in the management of COVID-19.
Remdesivir. See section 3.4
Oseltamivir inhibits neuraminidase, which influenza viruses use to replicate and spread. Coronaviruses do not use neuraminidase so oseltamivir has no activity against coronaviruses. Oseltamivir should be reserved for treating confirmed or suspected influenza. If started, it should be ceased if influenza is excluded.
A number of other antivirals are being investigated for activity against coronaviruses:
- Being evaluated in vitro for potential activity against coronavirus.
- Favilavir (also known as favipiravir)
- Published evidence is limited to two open-label trials with significant limitations.
- Clinical studies are awaited.
- While one randomised controlled trial (against standard care) of 199 patients did not show a significant difference in time to clinical improvement, larger trials are under way.
- New molecules under development (e.g. EIDD-2801)
Overall, there are no published randomised controlled trials to support the use of these medicines to treat humans with suspected or confirmed COVID-19 infection.
Further, some studies show increased adverse reactions with the use of antivirals compared to standard care (e.g. nausea/vomiting/diarrhoea with lopinavir-ritonavir). Inappropriate use of antivirals places patients at risk of harm without demonstrated evidence of benefit.
|Biologics currently have no clear role in the management of COVID-19 outside a clinical trial setting.|
Biologics are being investigated for activity against coronaviruses:
- Severe COVID-19 is associated with a marked inflammatory response, which may be the basis of the inflammatory lung damage. Anakinra is a recombinant protein similar to the endogenous interleukin 1 receptor antagonist protein, and therefore reduces interleukin-1 mediated inflammation. The clinical data for COVID-19 is sparse. Preliminary findings from case series and cohort studies are difficult to interpret. Until results from larger, randomised controlled trials are available, no conclusions can be drawn.
- IL-6 inhibitors (e.g. tocilizumab, sarilumab)
- IL-6 is a pleiotropic cytokine. A subgroup of patients with severe COVID-19 appear to develop features of a cytokine storm syndrome. It has been suggested that blocking the inflammatory pathway with an IL-6 inhibitor may prevent disease progression.
- Based on 4 published RCTs, tocilizumab was not found to have a survival benefit with mixed evidence for preventing mechanical ventilation. Patients included in these studies (n=889) had moderate to severe COVID-19, but were not in ICU.
- Preliminary results from the tocilizumab arm of the RECOVERY trial (n= 4116) found a survival benefit with tocilizumab in hospitalised patients with hypoxia and systemic inflammation. 29% (596/2022) of patients died within 28 days in the tocilizumab group compared to 33% (694/2094) in the usual care group (p=0·007). The benefit was seen regardless of the level of respiratory support and was additional to the benefits of systemic corticosteroids (e.g. dexamethasone).
- It is not known if blunting the immune response with tocilizumab will reduce longer term morbidity and mortality.
- Tocilizumab may be associated with an increased incidence of superinfections. Systematic review of tocilizumab use in rheumatoid arthritis found an increased risk of infectious respiratory adverse events.
- Interferons are biologic response modifiers that possess antitumour, antiviral, and immunomodulating properties. Interferons are virus specific, binding to specific receptors. Interferons have shown activity against coronaviruses in animal and in vitro studies. In a large retrospective cohort study, interferons were not effective against MERS-CoV. Current clinical trials include interferons in combination with antiviral agents for activity against COVID-19.
- Early trial results, from a double-blind, placebo-controlled trial, found that hospitalised patients with COVID-19 (n=101) who received inhaled interferon-beta had a lower risk of developing severe disease compared to placebo.
Protein and tyrosine kinase inhibitors (TKIs)
|Tyrosine kinase inhibitors (TKIs) currently have no role in the management of COVID-19.|
The safety and efficacy of TKIs for the treatment of patients with COVID-19 is not currently established through any published clinical trials. Baricitinib appears to be the preferred candidate in this class as it has been shown to reduce or interrupt the passage of virus into alveolar type 2 cells, and to inhibit JAK1- and JAK2-mediated cytokine release. Baricitinib is registered overseas for the treatment of rheumatoid arthritis. Two clinical trials are currently underway investigating baricitinib in the treatment of patients with COVID-19.
|Ivermectin currently has no role in the management of COVID-19.|
Published evidence for COVID-19 is limited to one in vitro study. To achieve the concentrations used in the in vitro experiment, potentially toxic doses of ivermectin would be required (based on both the physical and pharmacokinetic properties of ivermectin). Ivermectin has been used in a phase 3 clinical trial to treat dengue fever. In this trial ivermectin reduced serum concentrations of viral proteins but had no effect on viraemia or clinical outcomes.
The current evidence is insufficient to justify using ivermectin to treat COVID-19 outside a clinical trial setting.
|Nitazoxanide currently has no role in the management of COVID-19.|
The data for COVID-19 is limited to one in vitro study. Nitazoxanide has been used in a placebo-controlled RCT for patients hospitalised with influenza-like illness (n=260); nitazoxanide did not reduce the duration of hospital stay or confer other benefits.
The current evidence is insufficient to justify using nitazoxanide to treat COVID-19 outside a clinical trial setting.
|Acetylcysteine currently has no role in the management of COVID-19.|
Studies suggest acetylcysteine inhibits formation of proinflammatory cytokines in some strains of influenza. The activity of acetylcysteine is likely to be dependent on the strain of virus. There are no studies showing that acetylcysteine is effective against COVID-19 therefore, we do not recommend its use.
Bacillus Calmette-Guérin (BCG) vaccine
|The BCG vaccine currently has no role in the prevention of COVID-19.|
Published evidence from randomised controlled trials and observational studies has shown that BCG vaccination prevents non-tuberculous respiratory infections such as pneumonia and influenza, in children and the elderly. This relates to the non-specific effects of the BCG vaccine on the immune system. These effects have not been well characterised and their magnitude and duration is unknown.
There is a lack of evidence that BCG vaccine protects against COVID-19. However, two clinical trials are ongoing to determine if BCG vaccination protects healthcare workers against COVID-19.
|There are no clinical studies to support the use of oral vitamin C supplementation in the prevention of COVID-19.|
There is currently insufficient evidence to support the use of vitamin C, via any route, in the management of COVID-19. Clinical trials using intravenous high-dose vitamin C in patients hospitalised with COVID-19 are underway.
Two recent open-label studies on the use of intravenous high-dose vitamin C in other types of infections associated with septic shock and acute respiratory distress syndrome (ARDS) infections showed there was no clear benefit of vitamin C. Septic shock and ARDS are conditions leading to ICU admission, ventilator support or death among those with severe COVID-19.
|Vitamin D has no role in the management of COVID-19.|
Results from an RCT (n=240), did not find any clinical benefits associated with a single high dose of vitamin D3 in hospitalised patients with COVID-19. The median length of hospital stay for both the vitamin D3 (n=120) and placebo (n=120) groups was 7 days. There was also no difference in mortality, ventilation or ICU admission rates.
Vitamin D supplementation is only recommended for patients with documented deficiency, or the usual patient groups who are at risk of deficiency such as elderly people in residential care.
|Zinc supplements currently have no role in the prevention or treatment of COVID-19.|
We found no published reports of zinc being used to prevent or treat COVID-19 infection. The role of zinc is based on a number of theories, including the finding from an in vitro study in 2010 that zinc inhibited RNA-dependent polymerase replication of SARS-CoV virus. The evidence that zinc lozenges can reduce the severity of common cold symptoms is weak and inconsistent.
The evidence to support the use of zinc in the management of COVID-19 is theoretical only and we do not recommend its use. Clinical trials using zinc and other vitamin supplements in COVID-19 have been registered.
Complementary and Alternative Medicines
|Complementary and Alternative Medicines have no role in the prevention or treatment of COVID-19.|
A broad range of complementary and alternative medicines, including herbal products and dietary supplements, have been proposed for prevention and treatment of COVID-19. There is no evidence to support these claims. Additionally, these products pose several risks:
- They are unregulated and therefore of uncertain quality
- They risk unnecessary adverse effects and drug interactions
- They potentially reduce adherence with effective prevention (such as handwashing) by providing false reassurance
- Effective supportive treatments, such as paracetamol, may be deferred
- They are a preventable financial burden to patients
Complementary and alternative medicines are therefore not recommended for prevention or treatment of COVID-19.
|Famotidine currently has no role in the management of COVID-19.|
Retrospective observational data from Wuhan, combined with computerised modelling data, has led to a theory that famotidine may inhibit an enzyme involved in viral replication. An RCT in hospitalised patients with COVID-19 is underway, using high dose intravenous famotidine. Until the study results become available, we do not recommend the use of famotidine in COVID-19.
|Povidone-iodine gargle has no role in the management of COVID-19.|
An in vitro study suggests that povidone-iodine gargle reduces viral load (including MERS-CoV and SARS-CoV) in the oral cavity and the oropharynx, which could indicate that it might help prevent viral transmission. This study was funded by a pharmaceutical company. The clinical relevance has not been established.
The role of povidone-iodine in COVID-19 is as a topical disinfectant within standard infection control protocols.
|Melatonin currently has no role in the management of COVID-19.|
Melatonin has been identified as a potential medicine that could be repurposed for use in COVID-19 from a retrospective study using data from a COVID-19 registry.
Analysis of 26,779 people, of whom 8,274 tested positive for COVID-19, found that people who were taking melatonin were 28% less likely to test positive for COVID-19. The observational nature of the study means confounding may have contributed to the finding.
The current evidence is insufficient to justify the use of melatonin for treating COVID-19 outside a clinical trial setting. Several RCT’s are evaluating the clinical benefits of melatonin in patients with COVID-19.
Medicines reported to worsen COVID-19
|There are no clinical studies showing increased harm from any medicine use in relation to COVID-19. Patients should be advised not to stop any regular medicines unless there is a conventional indication to do so.|
COVID-19 uses angiotension-coverting enzyme 2 (ACE2) to enter cells. There is pre-clinical data from in vitro and animal studies that some medicines may upregulate ACE2, raising concerns that these medicines could increase the severity of COVID-19 infection. However, there are no clinical data (including the publications from the large number of cases in China) to support this theory.
Immunosuppression theoretically increases the risk of coronavirus infection but there is no clinical evidence to support this.
Some medicines are associated with pneumonia or respiratory depression, but the risk is too small or uncertain to justify altering usual prescribing of these agents.
Angiotensin Converting Enzyme Inhibitors (ACEIs) and Angiotensin Receptor Blockers (ARBs)
|Patients already taking ACEIs or ARBs should continue them unless there is a conventional reason not to (e.g. hyperkalaemia, acute kidney injury).|
ACEIs and ARBs upregulate ACE2 in animal studies (see above). ACE2 receptors have been shown to be the entry point into human cells for SARS-CoV-2. However, it is not clear that ACEIs or ARBs upregulate ACE2 in humans. Additionally, observational data to date shows no increase in mortality for patients taking ACEIs or ARBs when infected with COVID-19. There are also theoretical benefits to ACEIs and ARBs for viral infection, and very weak observational data supporting these. There are multiple clinical trials investigating these agents for the treatment of COVID-19.
We support the current consensus in New Zealand and internationally (for example European Medicines Agency, International Hypertension Society, American College of Cardiology) to continue normal usage of ACEIs and ARBs. The usual contraindications and cautions still apply, for example patients with hyperkalaemia or hypotension.
|Patients already taking thiazolidinediones (e.g. pioglitazone) should continue them unless there is a conventional reason not to (e.g. heart failure, history of bladder cancer).|
Thiazolidinediones, such as pioglitazone, upregulate ACE2 in animal studies (see above). Observational studies of patients with COVID-19 have shown increased hospitalisation and mortality for patients with diabetes (7.3% vs 0.9%). Reports have suggested this could be due to ACEI and ARB use, however there are no data to substantiate this. Diabetes has separately been shown to upregulate ACE2 and increases the risk of other infections, both of which add to the confounding in the observational data.
The usual contraindications and cautions still apply to ACEI and ARB use as they did prior to COVID-19, for example patients with heart failure or a history of bladder cancer. We recommend clinicians continue usual practice around the use of pioglitazone during the COVID-19 pandemic.
Nonsteroidal Anti-inflammatory Drugs (NSAIDs)
NSAIDs can be used in patients with COVID-19 in the same way as in other similar patient groups. Use the lowest possible dose for the shortest possible time.
There has been longstanding concern about possible harm from NSAIDs in viral infections. Randomised controlled trials and observational data comparing NSAIDs and paracetamol have produced mixed results with some showing no difference and others a small effect of NSAIDs. Overall, the data do not give a clear signal to draw a convincing conclusion.
In COVID-19 concerns were raised partly because of the potential for NSAIDs to upregulate ACE2 in animal models. In a population based cohort study the use of NSAIDs was not associated with increased risk in patients with COVID-19. This includes similar 30-day mortality and adverse outcomes (hospitalisation, ICU admission, mechanical ventilation, or renal replacement therapy) in NSAID users and non-users. NSAID use was defined as a filled prescription for an NSAID up to 30 days prior to the date of a positive COVID-19 test. See, cohort study.
The usual contraindications and cautions apply to NSAID use e.g. renal impairment, heart failure or increased risk of gastrointestinal bleeding.
|Patients should continue immunosuppressants while they remain well, even after potential COVID-19 exposure.|
We refer to immunosuppressants as any medicine dampening immune response, including those described as “immunomodulatory” rather than immunosuppressive. Examples of these medicines include corticosteroids, Disease Modifying Anti-Rheumatic Drugs (DMARDs), and monoclonal antibodies that affect the immune system.
Immunosuppressants theoretically increase the chances of contracting coronavirus, or developing more severe infection. However, the extent of this effect is uncertain. Ceasing immunosuppressants could destabilise control of the underlying disease resulting in direct patient harm from disease, risk of hospitalisation (and COVID-19 exposure), and use of more immunosuppressing regimens (such as high-dose corticosteroids) to regain disease control. The long duration of effect of most immunosuppressants means omitting doses after COVID-19 exposure, for example, confers little or no short-term reduction of immunosuppression.
The management of immunosuppression for patients with an active infection is dependent on individual factors, such as the indication for immunosuppression and severity of the infection. It is therefore not possible to provide explicit guidance here, but clinicians are advised to use the same approach as applies to other significant viral infections, such as influenza. Discussion with the relevant specialist is recommended.
|Patients taking antipsychotics should continue to take them unless there is a conventional reason to stop (e.g. falls or sedation).|
Antipsychotics are associated with an almost 2-fold increase in risk of pneumonia in observational studies. However, depending on the baseline risk of pneumonia the number needed to treat to cause one case of pneumonia is between 86 and over 1,126. The risk is much lower than other significant adverse effects of antipsychotics. A causal relationship between antipsychotics and pneumonia has not been definitively established.
Antipsychotic cessation could result in withdrawal or destabilisation of the underlying condition. Therefore, we do not advocate changing antipsychotic prescribing solely on the basis of COVID-19 risk.
Proton pump inhibitors (PPIs)
|Patients taking PPIs should continue to take them unless there is a conventional reason to stop (e.g. hyponatraemia or acute kidney injury).|
Large meta-analyses of observational studies and randomised trials have demonstrated an association between PPIs and pneumonia with an approximately 1.5-fold increase in risk. The effect appears greatest in the first month of treatment. Randomised data suggests a causal relationship.
The absolute increase in risk, however, is small. PPI cessation could result in worsening reflux (through withdrawal or reduced acid suppression) when PPIs are used for treatment, or gastrointestinal bleeding when PPIs are used prophylactically. Therefore, we do not advocate changing PPI prescribing solely on the basis of COVID-19 risk.
Selective serotonin reuptake inhibitors (SSRIs) and serotonin–noradrenaline reuptake inhibitors (SNRIs)
|Patients taking SSRIs/SNRIs should continue to take them unless there is a conventional reason to stop (e.g. fatigue or nausea).|
A single observational study has suggested a small increase in respiratory infections in older patients with COPD newly prescribed SSRIs or SNRIs. This has not been studied in other populations, and a causal relationship has not been established.
SSRI/SNRI cessation could result in withdrawal and/or destabilisation of the underlying condition. Therefore, we do not advocate changing SSRI or SNRI prescribing solely on the basis of COVID-19 risk.
|Patients taking anticholinergic medicines, such as oxybutynin, should continue to take them unless there is a conventional reason to stop (e.g. falls or sedation).|
Several observational studies of older adults have demonstrated an association between anticholinergic medicines and pneumonia. The extent of the effect is unclear due to variability in study results and design. A causal relationship between anticholinergic medicines and pneumonia has not been definitively established.
Anticholinergic cessation could result in withdrawal and/or destabilisation of the underlying condition. Therefore, we do not advocate changing anticholinergic prescribing solely on the basis of COVID-19 risk.
Patients taking long term opioids should continue to take them unless there is a conventional reason to stop (e.g. opioid toxicity).
Opioids may be useful for acute dyspnoea from COVID-19 in palliative patients.
Chronic opioid use is appropriate in some circumstances, including for patients with advanced lung disease and chronic, refractory dyspnoea. In these circumstances, respiratory depression is very rare. There is no evidence to suggest that this risk is increased in acute respiratory infections. Opioid cessation risks withdrawal and worsening of the underlying condition. We therefore do not recommend changes to chronic opioids solely on the basis of risk of COVID-19.
Opioids may be beneficial for acute dyspnoea, although studies supporting this are lacking. The frequency of respiratory failure with acute opioid use for dyspnoea is poorly characterised; it is likely to be rare but more common than with chronic use. Consensus guidelines support the use of opioids for dyspnoea in palliative care, but there are no guidelines advocating for or against opioids to treat acute dyspnoea outside of a palliative setting.
Other medicines associated with respiratory depression
|Patients should be advised not to stop any regular medicines unless there is a conventional indication to do so.|
Gabapentinoids (gabapentin and pregabalin) are rarely associated with respiratory depression, irrespective of concomitant medicines. There is no evidence to suggest that this risk is increased in acute respiratory infections.
Benzodiazepines are associated with respiratory depression and developing pneumonia in observational studies, and this may be worse with underlying lung disease. The precise extent of the risk is unclear. Zopiclone is associated with respiratory depression although there is weak evidence that the extent is less than that of benzodiazepines. There is no evidence to suggest that this risk is increased in acute respiratory infections.
Cessation of all of these medicines is associated with withdrawal and worsening of the underlying condition. We therefore do not recommend changes to prescribing of these medicines solely on the basis of risk of COVID-19.
Medicines monitoring in COVID-19
There is currently no need to deviate from standard monitoring requirements.
Anyone on clozapine showing signs of infection, including COVID-19, requires an urgent CBC
See HealthPathways: Clozapine Monitoring (includes a link to patient information).
Vaccines to prevent COVID-19
|There are many COVID-19 vaccine candidates undergoing clinical trials.|
The types of vaccine products under development include: RNA, DNA, viral vectors, peptides, virus-like particles, recombinant proteins, live attenuated viruses and inactivated viruses.
Two messenger RNA vaccines (Pfizer/BioNTech and Moderna) and one viral vector vaccine (AstraZeneca/University of Oxford), have preliminary data from Phase 3 trials suggesting 70-95% efficacy. All require two doses; however, it is unclear how long immunity will last.
See Immunisation Advisory Centre for COVID-19 vaccine information and resources.
|Links to general guidance and emerging evidence from clinical trials:|
Hospital HealthPathways: for local guidance and resources.
Ministry of Health: support for healthcare professionals and the public.
Health Quality and Safety Commission: support for healthcare professionals.
Australian COVID-19 Clinical Evidence Taskforce: support for healthcare professionals.
Centre for Evidence-Based Medicine/University of Oxford: for evidence reviews.
Cochrane Library: for evidence reviews.
National Institute for Health and Care Excellence (NICE): for guidance and resources.
COVID-NMA: for trial information and evidence reviews.